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by: Kenya Bernier I

Microorganisms&HumanDisease MBI111

Marketplace > Miami University > Microbiology > MBI111 > Microorganisms HumanDisease
Kenya Bernier I
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This 0 page Class Notes was uploaded by Kenya Bernier I on Sunday November 1, 2015. The Class Notes belongs to MBI111 at Miami University taught by JosephCarlin in Fall. Since its upload, it has received 36 views. For similar materials see /class/233341/mbi111-miami-university in Microbiology at Miami University.


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Date Created: 11/01/15
COMMON DISEASES TRANSMITTED BY SKIN INFECTION SOILBORNE DISEASES ANTHRAX agent Bacillus anthrasis gram sporeforming rod B anthrasis in blood slide JMC historical significance first microbe to be proven a cause of disease first grown in pure culture first to satisfy Koch39s postulates among first used for immunization primarily a disease of large animals spores remain in carcass transmission inhalation of spores while grazing must cremate or bury body burn field pathogenesis spores rapidly germinate on contact with tissue capsule inhibits phagocytosis produces several toxins organs fill with bloody black fluid 80 mortality human diseases pulmonary anthrax woolsorters disease acquired by wool sheep and hide workers transmission inhalation of spores rapid and severe blood infection extensive hemorrhaging hemorrhagic pneumonia SOILBORNE DISEASES ANTHRAX gastrointestinal anthrax rare in humans transmission ingestion of contaminated meat lesions on intestinal wall blood invasion violent dysentery anthrax of skin transmission contact with contaminated animal products boillike lesions with black crusts blood invasion anthrax lesion slides 303 304 treatment penicillin must be given early vaccine exists a potential agent of biological warfare SOILBORNE DISEASES TETANUS TETANUS agent Clostridium tetani gram anaerobic sporeforming rod CI tetani gram stain slide MB 45 CI tetani EM slide JMC transmission wound entry revert to vegetative bacilli in anerobic environment pathogenesis no invasiveness can live in intestine without causing disease tetanospasmin toxin second most powerful after botulinum toxin inhibits removal of acetylcholine from synapse results in continuing nerve impulses spastic paralysis synapse slide JMC symptoms develop within hours muscle stiffness facial and swallowing muscles clenching of teeth lockjaw arching of back seizures in diaphragm and rib muscles paralysis slide BB89 treatment penicillin antitoxin muscle relaxants and sedatives immunization DPT tetanus toxoid formaldehydetreated toxin boosters every ten years SOILBORNE DISEASES GAS GANGRENE GAS GANGRENE gangrene condition that develops when blood flow ceases to a local area usually by blockage with dead tissue body part becomes dry shrunken and purpleblack may spread as proteolytic enzymes are released from dead cells aka dry gangrene gas gangrene occurs when soilborne bacteria invade dead anaerobic tissue aka moist gangrene clostridial myonecrosis agent Clostridium perfringens and other Clostridium sp gram sporeforming rods transmission introduction of spores into anaerobic tissue battle wounds surgery abortion earpiercing dental extraction pathology rapid multiplication ferment muscle carbohydrates putrefy proteins gas production further destroys tissue enzymes destroy tissue neurotoxins produced symptoms intense pain and swelling at wound site foul odor gas gangrene slide JMC site turns red gt green gt blueblack toxin damage to heart and nervous system CONTACT BACTERIAL DISEASES LEPROSY LEPROSY HANSEN39S DISEASE o leprosy has been with humanity for thousands of years note ancient bans on lepers in Jewish and Old Testament writings o in Europe 400 AD special houses were set aside for lepers as the Roman government became Christian it adopted biblical injunctions about treatment of persons with disfiguring skin diseases this is probably where our concept of quarantine arose o leprosy became well established in Europe France and Britain and the Mediterranean coastlands Egypt during 6th century AD 0 prevalence of this disease declined greatly during the 14th century plague and tuberculosis were on the upswing then Was leprosy was simply outcompeted by quotquickerquot pathogens agent Mycobacterium Ieprae acidfast rod first observed by Hansen in 1874 hence Hansen s disease not yet cultivated in artificial medium Koch s postulates not fulfilled animal model armadillos transmission multiple skin contacts droplets incubation period 36 years makes identification difficult CONTACT DISEASES LEPROSY symptoms organism is heat sensitive symptoms occur in cooler extremities skin and nervous system of hands feet face eanobes eyes and respiratory tract if severe two forms of the disease exist different sets of symptoms due to differing immune responses lepromatous leprosy disfigurement of skin and bones twisting of limbs curling of fingers claw hand loss of facial features thickening of outer ear collapse of nose quotamputations slide BB38 lepromas on skin and respiratory tract tumorlike growths lepromatous leprosy slide BB34 tuberculoid leprosy loss of pain sensation victims suffer unknowingly physical damage tuberculoid leprosy slide BB39 CONTACT DISEASES LEPROSY treatment dapsone a sulfa drug resistance is emerging diagnosis lepromin test similar to tuberculin test positive in tuberculoid leprosy negative in lepromatous leprosy incidence over 10 million cases worldwide 100 in US CONTACT DISEASES STAPH SKIN INFECTION STAPHYLOCOCCAL SKIN DISEASES agent Staphylococcus aureus gram coccus normal skin mouth nose throat inhabitant transmission penetration open wounds hair follicles earpiercing dental extractions symptoms abscess a circumscribed pusfilled lesion boil skin abscess can begin as a pimple boil slide JMC carbuncle penetration to deeper tissue scalded skin syndrome seen in infants skin becomes red wrinkled and dry may peel off high mortality if untreated caused by exotoxin scalded skin slide JMC impetigo contagiosum more superficial than 888 thin walled blisters in patches of epidermisjust below skin surface impetigo slide JMC treatment antibiotics simple boil can lead to septicemia other systemic effects and food poisoning symptoms CONTACT DISEASES STAPH TOXIC SHOCK TOXIC SHOCK SYNDROME TSS blood disorder characterized by sudden fever and circulatory collapse outbreak in late 197039s most cases due to introduction of new more absorbent tampons prompt detection of the epidemic and determination of the predisposing factors involved manufacturers rapidly withdrew the problem tampons from the market and essentially eliminated the epidemic nevertheless 174 cases were reported in the US during 1999 agent toxin producing strain of S aureus symptoms rapidly rising fever vomiting and diarrhea sore throat myalgia sunburnlike rash and skinpeeling on palms and soles sudden drop in blood pressure treatment antibiotics and blood transfusion to assist shock incidence 200 casesyear tampon use may lead to environment favoring growth and toxin production not limited to tampon users surgical dressings sometimes implicated GASTROINTESTINAL INTOXICATIONINFECTION INTOXICATION INTOXICATIONS diseases in which bacterial toxins are ingested in food and water STAPHYLOCOCCAL FOOD POISONING may be most common type of food poisoning agent Staphylococcus aureus gram positive coccus grows in clusters S aureus gram stain slide MB 1 disease caused by exotoxin produced in foods during bacterial growth incubation period 16 hour symptoms restricted to intestine gt enterotoxin cramps nausea projectile vomiting prostration diarrhea lasts a few hours then rapid recovery pathogenesis enterotoxin toxin is among most heatresistant of all exotoxins resists 100 C20 min no obvious taste odor or appearance S aureus grows from 8 45 C psychrotrophic can sometimes produce toxin in refrigerator can be in spoiled meats dairy products creamfilled pastries potato salad and coleslaw mayonnaise INTOXICATION STAPH FOOD POISONING reservoir nasal cavity sneeze or more commonly from an abscess phagetyping can be performed to identify strains phage typing slide JMC INTOXICATION CLOSTRIDIAL FOOD POISONING CLOSTRIDIAL FOOD POISONING second most common following staphylococcal food poisoning agent Clostridium perfringens agent of gas gangrene gram anaerobic sporeforming bacillus can contaminate proteinrich foods meat poultry beans if spores survive cooking germinate and produce enterotoxin in anaerobic portions of food outbreaks result from failure to refrigerate cooked meats promptly incubation 814 hours longer than staph symptoms cramps abdominal pain profuse watery diarrhea vomiting and nausea rare rapid recovery therapy not required INTOXICATION BOTULISM BOTULISM agent Clostridium botulinum gram positive anaerobic sporeforming bacillus C botulinum spore stain slide MB 48 disease caused by exotoxin produced in foods during bacterial growth incubation 14 days symptoms blurred or double vision slurred speech difficulty swallowing and chewing labored breathing limbs lose tone flaccid paralysis may resemble stroke GuillainBarr syndrome myasthenia gravis pathogenesis preformed toxin is absorbed into bloodstream affects nervous system gt neurotoxin bacteria of little consequence don t grow in intestine powerful neurotoxin 1 pint would kill entire world population 1 ounce would kill all in US toxin penetrates end brushes of nerve cells inhibits release of acetylcholine into nervemusclejunction l no nerve impulse to muscle gt no contraction l respiratory paralysis and death INTOXICATION BOTULISM synapse slide JMC reservoir spores intestines of man and animals manure sewage organic fertilizers harvested products spores enter anaerobic environment ofjars and cans germinate bacilli produce exotoxin contaminated cans lack evidence of toxin no production of gas and canswelling food smells and tastes normal treatment antitoxin antibiotics of no use WHY identification by neutralization studies in animals prevention heat food before consumption 90 C for ten minutes most cases related to cold foods wound botulism in anaerobic wounds infant botulism growth of organism in infant s intestine occurs before other competing normal flora established may be related to sudden infant death syndrome SIDS GASTROINTESTINAL INTOXICATIONINFECTION INFECTIONS INFECTIONS diseases in which microbes ingested in food or water grow in the body VIRAL GASTROENTERITIS agent a general name for the disease caused by several viruses rotavirus family Reoviridae most frequent segmented ds RNA inner and outer capsids Norwalk virus enteroviruses Coxsackie virus may be the 24hour bug echovkus gnteric cytopathogenic human grphan virus transmission food and water symptoms explosive onset diarrhea nausea vomiting lowgrade fever cramps headache malaise particularly severe in highrisk patients complications dehydration and meningitis INFECTIONS VIRAL GASTROENTERITIS vaCCI ne only for rotavirus incidence 130 million cases in children worldwide 3 million in US 875000 deaths 20100 in US INFECTIONS ENTERITIS SALMONELLOSIS also called gastroenteritis or enteritis most reported of all foodborne diseases in US 40500 in 1999 agent several species including 5 enteriditis S typhimurium S heidelberg and S newport gram negative rods Salmonella sp gram stain slide MB 800 transmission enter intestine in foods incubation 13 days symptoms same as viral gastroenteritis may last 1 week mild ulceration and rare blood invasion treatment disease allowed to run its course no antibiotics fluid replacement may be necessary dehydration diagnosis isolation from stool reservoir unpasteurized milk undercooked poultry eggs custards eggnog ice cream mayonnaise certain live animals baby chicks and turtles snakes turtle slide BD 65 INFECTIONS ENTERITIS TYPHOID FEVER agent Salmonella typhi gram rod Salmonella sp EM slide JMC resistant to environmental conditions can survive in water sewage and certain foods acidresistant survives stomach pH transmission 5Fs flies food fingers feces and fomites oralfecal route symptoms invades small intestine causes deep ulcers and bloody stools no diarrhea invades blood after few days fever lethargy delirium rose spots on abdomen blood hemorrhaging rosespots slide MC 351 can get bowel perforation and gall bladder infection diagnosis culture from blood and stools Widal test agglutination of S typhi by patient serum Ab produced treatment with antibiotics resistance due to R factors INFECTIONS TYPHOID FEVER reservoir humans as carriers 5 continue to shed organisms after recovery quotTyphoidquot Mary Mallon 18701938 a cook caused more than a dozen typhoid outbreaks she was a carrier of Salmonella typhi she kept this up from 19001915 George Soper epidemiologist recognized Mallon as common source in epidemics tracked her down had her arrested and quarantined Mallon died injail from pneumonia vaccine exists but not very effective INFECTIONS ENTERITIS TYPHOID AND DYSENTERY transmitted by fecaloral contact these have plagued humans for millennia these diseases frequently affect soldiers due to poor sanitation 0 Battle of Crecy in 1346 the French waited to shoot the British riddled with dysentery until they were squatting defenseless 0 Prince Edward died of dysentery during the Hundred Years War Britain was forced to deal with the bubonic plague under the leadership of ten yearold Richard II who abdicated and starved himself to death in prison 0 during the Civil War 18611865 81360 men died of typhoid or dysentery 186216 men died of other diseases 93443 men died of wounds 0 when sanitation engineering was introduced late in the 19th century civilian deaths due to these diseases plummeted once soldiers were ordered to drink only boiled water their death toll due to these diseases also dropped 0 World War II first war in which the death due to wounds was greater than deaths due to infectious disease INFECTIONS ENTERITIS SHIGELLOSIS BACTERIAL DYSENTERY dysentery waves of intense cramps passage of frequent smallvolume bloody mucoid stools agent Shigella species S sonnei S dysenteriae S exneri and S boydii small gram rods found primarily in primates Sh dysenteriae gram stain slide MB 950 transmission contaminated water eggs vegetables shellfish dairy products incubation 23 days acidresistant ingest lt1000 organisms symptoms disease can range from mild diarrhea to fatal dysentery microbes penetrate intestine produce enterotoxins gt water released from intestinal lining infection in small intestine gt watery diarrhea infection in large intestine gt dysentery shigellosis bowel slide 30 72 usually lasts 1 week if no complications treatment antibiotics can be used many strains resistant R factors excessive fluid loss requires electrolyte therapy salt tablets or IV most often in children and elderly recovered are carriers for 1 month diagnosis culture from stool INFECTIONS DYSENTERY vaccine none INFECTIONS ENTERITIS CHOLERA agent Vibrio cholera curved gram negative rod vibrio 0 has caused trouble for people for centuries especially in Asia 0 in India religious rituals involve bathing in the Ganges River that is heavily contaminated with human feces containing V cholerae o it normally lives in water attached to the outer surfaces of crustaceansalgae it is ubiquitous cholera fluorescence slide JMC transmission contaminated water and food vegetables from fields fertilized with nightsoil shellfish effluent from aircraft pathogenesis sensitive to acid must ingest gt 10 million organisms to get colonization of intestine noninvasive enterotoxin produced gt loss of fluid from intestinal lining symptoms massive diarrhea up to 1 literhour for several hours ricewater stools colorless and watery sunken eyes skin wrinkled dry cold muscular cramps INFECTIONS CHOLERA blood thickens urine production ceases sluggish blood flow gt shock and coma cholera dehydration slide 30 16 cholera cot slide 30 17 treatment antibiotics and fluid therapy electrolytes fluid replacement is key to survival 70 mortality if untreated epidemiology occurs in pandemics vaccine exists for world travelers 6month protection prevention hygiene best for prevention INFECTIONS ENTERITIS E COLI D IARRH EAS agent by Escherichia coli gram negative rod infantile diarrhea enterotoxic strains produce enterotoxin similar to cholera toxin primarily in small intestine enteroinvasive strains penetrate intestinal epithelium like shigellosis primarily in large intestine both treated with antibiotics and fluid replacement traveler s diarrhea Montezuma s revenge caused primarily by enterotoxic by E coli other agents can be responsible hemolytic uremic syndrome HUS caused by enteroinvasive E coli0157H7 produces a ShigeIIalike toxin transmission undercooked beef hamburgers and raw milk symptoms spectrum of disease mild diarrhea gt severe bloody diarrhea hemorrhagic colitis hemolytic anemia and thrombocytopenia gt acute renal failure in children characterized by sudden onset of GI bleeding incidence 4500 cases in 1999 INFECTIONS ULCERS ULCERS HELICOBACTER PEPTIC DISEASE SYNDROME agent Helicobacter pylori curved gram negative rod transmission oral or fecaloral contact early in life infected 80 of people in developing countries 40 in developed countries are infected pathogenesis lives in gastric mucous moves toward gastric epithelial cells using flagella adheres by binding proteins produces urease neutralizes stomach acid induces inflammation cytotoxin damages gastric cells infiltrating phagocytes secrete cytokines that augment and prolong inflammation leading to formation of ulcers complications include up to 12Xincreased rate of gastric adenocarcinoma treatment combination Clarithromycin metronidazole antibiotics bismuth subsalycilate active ingredient in PeptoBismol rantidine Zantac prevention none that are effective PRINCIPLES OF DISEASE AND EPIDEMIOLOGY PRINCIPLES OF INFECTIOUS DISEASE INTERMICROBIAL RELATIONSHIPS symbiosis a situation in which two populations of organisms interact in a close and permanent association benefits food protection support other lifesustaining factors synergism two populations live together and accomplish what neither could alone mutualism benefits both organisms nitrogenfixing bacteria living in plant root nodules Fish mutualism light JMC dark JMC Lightemitting bacteria light JMC dark JMC Lactobacilus in vagina nutrients and production of acid environment commensalism one population benefits the other neither benefits nor is harmed ie normal flora bacteria that inhabit the skin bacteria that inhabit intestine E coli may actually be mutualistic supplies certain vitamins and metabolizes otherwise indigestible foodstuffs antagonism parasitism the relationship is beneficial to one organism harmful to the other bacteria that cause human disease are typical parasites PRINCIPLES OF INFECTIOUS DISEASE HOSTPARASITE RELATIONSHIP THE HOSTPARASITE RELATIONSHIP Infection the living together of host and parasite and the competition that takes place between them Disease any change from the general state of good health not all disease is infectious and infection does not always lead to disease normal flora microorganisms that infect without causing disease an example of symbiosis either mutualism or commensalism found in several tissues skin oral cavity upper respiratory tract intestine genitourinary tract introduced in the birth canal and gradually acquired from environmental exposure PRINCIPLES OF INFECTIOUS DISEASE HOSTPARASITE RELATIONSHIP pathogenicity the ability to enter host tissues and cause disease virulence the degree of pathogenicity of a parasite highly virulent cholera plague typhoid Ebola less virulent common cold viruses opportunistic little virulence until normal defenses are suppressed microbes seize the quotopportunityquot invade tissues and act as pathogens S pneumoniae can invade damaged lung tissue gt pneumonia in Ale Pneumocysz is Toxopasma Cryptosporidium applies to transplant patients and cancer victims in which immunosuppression is a result of treatment illustrates how shift in bodies controls can convert infection to disease loss of immune system gt opportunistic infection antibiotics can kill normal flora gt outgrowth of resistant organisms Candidiasis if Iactobacilli are eliminated PRINCIPLES OF INFECTIOUS DISEASE ESTABLISHMENT OF DISEASE ESTABLISHMENT OF DISEASE portal of entry site at which parasite enters host may be specific for certain organisms C tetanispore in wound but not in intestine S typhi in intestine not lung S pneumoniae in lung not intestine may be related to specific adhesive factors some organisms have multiple ports of entry M tuberculosis droplets contaminated food and milk skin wounds some require direct injection into bloodstream arthropodborne diseases dose the number of organisms that must be taken into the body to establish disease typhoid fever 1 million cholera many more typhoid bacillus is more resistant to acid pH of stomach exposure to low doses can sometimes result in immunity PRINCIPLES OF INFECTIOUS DISEASE VIRULENCE FACTORS VIRULENCE FACTORS adhesins factors that allow the colonization of a host gonococci attach by pili to specific receptors on tissues of urogenital system invasins factors that allow penetration tissues gt damage Falkow et al genes for cell penetration exist in certain bacteria isolated penetration genes of Yersinia pseudotubercuosis inserted them into E coli which allowed it to penetrate cells typhoid bacillus and amebas are invasive sharp appendicitislike pain not required for disease pertussis and cholera bacteria remain on surface toxins lead to the disease evasins factors that allow microbes to evade defenses specific enzymes can interfere with host defenses virulence factor overhead MKK 173 differing strategies of microbes coagulase clot sticks to staph and protects from phagocytosis coagulasepositive staph considered virulent streptokinase dissolves fibrin clot around strep toxins a microbial poison a single toxin can make an organism virulent two types exotoxins and endotoxins PRINCIPLES OF INFECTIOUS DISEASE VIRULENCE FACTORS toxins overhead MKK 172 exotoxinssecreted botulinum toxin among most lethal 1 pint could kill world population blocks nerve activity gt paralysis flaccid paralysis tetanus toxin blocks termination of nerve activity gt uncontrolled muscle contractions spastic paralysis diphtheria toxin interferes with protein assembly in upper respiratory tract gt accumulation of cell debris mucus bacteria fibrous material WBC gt respiratory blockage types of exotoxins neurotoxin affects nervous system enterotoxin affects GI tract antitoxins neutralizing antibodies to exotoxins can be used in treatment of botulism tetanus and diphtheria toxoid an altered toxin which is inactive yet still elicits an immune response formed by heat or chemical means can be used to immunize DPT vaccine endotoxins part of cell wall lipopolysaccharide layer symptoms are general fever weakness aches malaise cause damage to circulatory system alters permeability of blood vessels gt leaking of fluids endotoxin shock swollen tissues low blood pressure coma may accompany antibiotic therapy of gram organisms EPIDEMIOLOGY OF INFECTIOUS DISEASE PATTERN OF DISEASE PROGRESS PATTERN OF DISEASE PROGRESS progress of disease overhead Alcamo 173 incubation period time from parasite entry to appearance of symptoms cholera 13 days chickenpox 2 weeks leprosy 36 years period of prodromal symptoms general symptoms nausea fever headache malaise period of acme acute stage where specific symptoms appear scarlet fever skin rash hepatitis jaundice chickenpox vesicles period of decline gradual decrease in symptoms or rapid decline following crisis period of convalescence body39s systems return to normal EPIDEMIOLOGY OF INFECTIOUS DISEASE TYPES OF DISEASE TYPES OF DISEASE clinical disease symptoms are apparent measles and malaria subclinical disease few obvious symptoms acute develops rapidly accompanied by severe symptoms climaxes and fades quickly cholera epidemic typhus yellow fever chronic lingering disease slow development of symptoms rarely reach a climax convalescence may last months hepatitis A trichomoniasis infectious mononucleosis some acute diseases can become chronic when body is incapable of eliminating all parasites giardiasis amebiasis primary occurs in othenNise healthy individual secondary develops in weakened individual influenza as a primary disease can allow development of pneumonia as a secondary disease local restricted to a single area of body staphylococcal skin boil systemic disseminate to deeper organs and systems septicemiabacteremia spread of bacteria via blood stream fungemia viremia parasitemia EPIDEMIOLOGY OF INFECTIOUS DISEASE TRANSMISSION OF DISEASE TRANSMISSION OF DISEASE direct methods requires close or personal contact with infected individual handshaking kissing sexual intercourse contact with feces gonorrhea genital herpes intestinal disease exposure to droplets mucus expelled during cough or sneeze influenza measles pertussis streptococcal sore throat exposure to infected animals rabies indirect methods consumption of contaminated food or water poultry source of salmonellosis fomites inanimate objects that carry disease organisms bed linen pinworm eggs used syringes hepatitis and HIV vectors insects mechanical transports disease organism biological disease in organism yellow fever malaria RMSF Lyme disease transmission overhead Alcamo 174 reservoirs continuing sources of disease may be human animal water or soil carrier has recovered from disease but continues to shed organisms typhoid fever amebiasis communicable disease transmissible among hosts EPIDEMIOLOGY OF INFECTIOUS DISEASE TRANSMISSION OF DISEASE contagious pass among hosts with particular ease chickenpox measles genital herpes noncommunicable acquired directly from environment not easily transmitted to next host tetanus spores endemic occurs at a low level in a specific geographic area epidemic a disease that breaks out in explosive proportions in a population pandemic occurs worldwide RESPIRATORY INFECTION BACTERIAL STREPTOCOCCAL DISEASESUPPER RESPIRATORY TRACT encapsulated gram chainforming microbes strep gram stain slide MB 80 strep SEM JMC classification schemes hemolytic pattern hemolytic a and 3 pattern slides JMC beta alpha clear zone due to complete destruction green zone on blood agar due to incomplete hemolysis gamma no hemolysis Lancefield based on variants of carbohydrate in cell wall A 0 most disease by Group A strep S pyogenes is most common aka Group A Bhemolytic strep strep throat Group A strep transmission droplets invades pharynx as a primary disease incubation 13 days symptoms high fever swollen lymph nodestonsils bright red pharynx tissue strep throat slide 054386 MC slides RESPIRATORY INFECTION STREPTOCOCCUS M protein in cell wall and pili enhances attachment and inhibits phagocytosis 60 antigenic types scarlet fever Group A strep plus toxin strep throat along with a skin rash pinkred blush on neck chest part of arms scarlet fever rash slide JMC strawberry tongue slide JMC due to action of erythrogenic toxin capillary wall damage gt blood leaking toxin only produced by certain strains antibody to toxin provides immunity to scarlet fever rash not strep throat immune complications of strep throat 1 4 weeks after acute infection rheumatic fever characterized by fever inflammation of small blood vessels joint pain permanent scarring of heart valves valve damage Ab specific to strep Ag crossreacts with heart tissue cytotoxic hypersensitivity glomerulonephritis inflammation in kidney can cause permanent kidney damage RESPIRATORY INFECTION STREPTOCOCCUS other streptococcal diseases depends on portal of entry erysipelas disease spreads from wounds and abrasions red welldefined skin eruptions facial erysipelas slide 21bacterial diseases necrotizing fasciitis group A strep infected wounds extensive damage of soft tissue rapid spread septicemia blood poisoningquot from surgical or traumatic wounds puerperal sepsis septicemia spreads from uterus following child birth Group B strep genital tract infection in women pathogenesis premature labor infection in the newborn pneumonia septicemia meningitis prevention antibiotic treatment of infected women vaccine under development RESPIRATORY INFECTION PNEUMOCOCCUS PNEUMOCOCCAL PNEUMONlALOWER RESPIRATORY TRACT pneumonia microbial disease of the bronchial tubes and lungs 80 caused by Streptococcus pneumoniae encapsulated gram chainforming diplococci pneumococcus pneumococcus gram stain MB 201 pneumococcus india ink stain MB 200 transmission droplet and contact normal flora natural resistance is high often a secondary infection risk factors smoking malnutrition viral infections and immunosuppression affects all ages highest mortality in elderly or underlying medical conditions symptoms high fever sharp chest pains difficult breathing rustcolored sputum blood seeping into alveolar sacs from tissue damage lobar pneumonia involvement of entire lobe double pneumonia involvement of both lobes bronchopneumonia patches of infection in passageways otitis media middle ear infection in children treatment antibiotics resistance exists vaccine based on capsule polysaccharide 80 different strains based on capsule vaccine for pneumonia uses capsules of 23 strains vaccine for otitis media uses capsules of 8 strains provides protection against 90 of infections RESPIRATORY INFECTION TUBERCULOSIS TUBERCULOSISLOWER RESPIRATORY TRACT agent Mycobacterium tuberculosis small acidfast rod acidfast stain slide MB 155 0 transmission droplet multiple exposures usually required found in crowded living conditions incidence 17500 cases in 1999 pathogenesis in 10 disease occurs within three months cough chest pain high fever blood in sputum in 90 generalized symptoms malaise fever and weight loss body walls off organism WBCs calcium salts and fibrous material forms hard nodule called tubercle tubercle visible in chest Xray chest X ra y 9 1 bacterial diseases bacteria survive and tubercle can grow miliary TB bacteria spread from ruptured tubercle to a variety of organs millet seedlike lesions in organs miliary TB in lung slide 93bacterial diseases consumption growth is so unrelenting that tissue is consumed Pott s disease TB in spine of children RESPIRATORYINFECTION TUBERCULOSIS detection aided by TB skin test PPD type IV cellular hypersensitivity skin test slide JMC treatment antibiotics for 69 months antibiotic resistance is increasing 30 MDR worldwide vaccine BCG Bacille CalmetteGuerin strain of M bovis M aviumintracellulare cause lung disease and death in AIDS victims RESPIRATORY INFECTION HAEMOPHILUS HAEMOPHILUS MENINGITISUPPER RESPIRATORY TRACT agent Haemophilus influenzae thought at one time to be etiologic agent of influenza small encapsulated gram rod greatest cause of bacterial meningitis in US 18000 casesyr symptoms respiratory infection as a complication to previous infection in children between 6 mo and 2 yrs moves from respiratory tract gt blood gt meninges stiff neck severe headache neurologic symptoms listlessness drowsiness irritability 5 mortality 2030 permanent side effects hearing loss gt mental retardation treatment antibiotics resistance exists incidence 1300 cases invasive in 1999 vaccine HiB vaccine capsule polysaccharide of type B 95 of infections due to capsule B serotype RESPIRATORY INFECTION PNEUMOTROPIc VIRAL DISEASES INFLUENZA acute contagious disease of upper respiratory tract occurs in pandemics ie Asian flu Hong Kong flu Swine flu Spanish flu the pandemic of 19181919 started in the US spread like wildfire 1 it struck every state in the US army bases naval forces even prisons within a week in March then spread across the Atlantic to France by early April 2Japan and China were stricken by midApril Africa and South America by May transfer of military personnel back home from World War I played a major role in its transmission worldwide up to 90 of the population was ill in some areas Samoa death rates as high as 20 in the Pacific islands 60 among Eskimos 2537 million people died in 18 months time a world record for the largest number of people to die in a pandemic in the shortest time most of the victims actually died of pneumonia a secondary infection this strain of influenza virus disappeared in 1919 3 types A most pandemics B less widespread Cmm RESPIRATORY INFECTION INFLUENZA 9 other strains of this highly mutable virus continue to cause pandemics but none have come close to this quotclassicquot spikes in envelope serve as antigens hemagglutinin H facilitates attachment neuraminidase N assists entry and exit new drug target in uenza schematic slide JMC in uenza EM slide JMC RESMRATORYINFECHON INFLUENZA antigenic variation antigenic drift chemical changes mutation in H and N results in different strains antigenic shift recombination of genes between flu strains avian and human flu antibodies produced during a prior infection are ineffective against the new strain results in another infection upon exposure precludes the development of a universal vaccine in uenza overhead Alcamo 121 nomenclature is based upon the antigenic variant present ie AH3N2 symptoms sudden chills fatigue headache pains in chest back and legs fever rises to 104 F severe cough develops obstructed nose dry throat tight chest viral invasion of trachea and bronchi stomach flu is a misnomer prognosis favorable normally shortlived selflimiting 710 days can lead to secondary infections RESPIRATORY INFECTION INFLUENZA diagnosis symptoms and pattern of spread in community virus isolation in laboratory agglutination of type 0 RBCs treatment amantadine interferes with attachment and uncoating new drugs under development target neuraminidase vaccine inactivated virus can protect highrisk population based on predicted strain outbreak for each flu season complications GuillainBarr syndrome nerve damage paralysis and coma follows recovery or immunization Reye s syndrome in children during recovery from flu or chickenpox rising fever repeated protracted vomiting child becomes lethargic glassyeyed disoriented incoherent and combative liver and brain damage coma and death possible Reye s overhead Alcamo 122 thought to be related to immune system linked to administration of aspirin RESPIRATORY INFECTION ADENOVIRUS ADENOVIRUS INFECTIONS named from adenoid tissue from which originally isolated at least 31 types icosahedral DNA ds virus EM slide adenovirus panel d JMC form inclusions in host cells a crystalline array of viruses upper respiratory infection common coldsore throat distinctive symptoms substantial fever sore throat pharyngitis severe cough swollen lymph nodes of neck whitishgray material appears over throat effects may be long lasting keratoconjunctivitis inflammation of cornea and conjunctiva reduced vision for several weeks with spontaneous recovery transmission droplet contact water swimming pool conjunctivitis fomites ophthalmic instruments RESPIRATORYINFECTION ADENOVIRUS viral meningitis aseptic meningitis no visible agent inflammation of the membranes of the brain or spinal cord RESPIRATORY INFECTION HANTAVIRUS HANTAVIRUS ACUTE RESPIRATORY DISEASE SYNDROME ARDS carrier rodents transmission inhalation of aerosolized virus in rodent droppings and urine incidence 33 cases in 1999 in USA upper respiratory tract infection initially mild and flulike fever and cough gt capillaryleak syndrome massive fluid accumulation in lungs gt 4050 mortality Four Corners outbreak due to increase in rainfall gt more crops gt more mice deer mouse slide JMC in Asia hemorrhagic fever with renal syndrome Hantaan upper respiratory gt kidney involvement initially flulike gt hemorrhages under skin gt internal hemorrhaging gt kidney failure gt 10 mortality annual outbreaks coincides with harvest farmers disturb rodent burrows and inhale virus in rodent urine RESPIRATORY INFECTION RHINOVIRUS RHINOVIRUS INFECTIONS rhinovirus rhinos nose over 100 different viruses upper respiratory infection major cause of common cold head cold symptoms headache chillsdry scratchy throat runny nose and congestion cough variable fever absent or slight sometimes croup hoarse coughing thrive in human nose slightly lower temperature vaccine prospects not promising due to the diversity of viruses that cause colds may be easier to interrupt transmission by nonspecific means 16000 virus shedsneeze rhinovirus recovered from hands of 50 of cold sufferers shaking hands with infected individual more risky than kissing RESPIRATORY INFECTION DERMOTROPIC VIRAL DISEASES CHICKENPOX VARICELLA 3nd most reported disease in US 46000 annually down from 185000 in 1989 family Herpesviridae DNA icosahedral ds envelope transmission droplet and contact among most communicable incubation 2 weeks symptoms early fever headache malaise upper respiratory tract gt bloodstream gt peripheral nerves and skin formation of fluid filled vesicles chickenpox lesion slide JMC chickenpox patient slide JMC develop over 34 days in cropswaves itch intensely nerve involvement break open to yield virusladen fluid eventual crusting and healing mortality low complications Reye s syndrome RESPIRATORY INFECTION VARICELLAZOSTER pneumonia encephalitis bacterial infection of skin vaccine newly approved Varivax contributing to declining numbers of cases SHINGLES HERPES ZOSTER agent same virus as chickenpox transmission reactivation of latent virus multiply in nerve ganglia and travel down nerves to trunk symptoms cause blisters with blotchy patches of red encircling trunk shingles lesion slide JMC shingles slide JMC epidemiology linked to stress and immunosuppression usually occurs in people over age 50 RESPIRATORY INFECTION MEASLES RUBEOLA MEASLES RUBEOLA agent family Paramyxoviridae RNA helical envelope with hemagglutinin spikes related to mumps and RS viruses transmission droplet symptoms hacking cough sneezing nasal discharge eye redness sensitivity to light high fever Koplik spots two days after onset red patches with white grainlike centers Koplik spot slide JMC red rash two days after Koplik spots begins at hairline gt face gt trunk and extremities resembles rash of scarlet fever no sore throat measles rash slide JMC X2 complete recovery within a week of rash complications subacute sclerosing pancephalitis SSPE RESPIRATORY INFECTION MEASLES RUBEOLA fatal degenerative brain disorder occurs years after initial infection vaccine attenuated virus MMR incidence 100 cases in 1999 RESPIRATORYINFECTION MUMPS MUMPS characterized by swollenjaw tissues from swollen salivary glands particularly the parotid glands family Paramyxoviridae RNA helical envelope with hemagglutinin spikes transmission droplets contact fomites virus is found in blood urine and CSF effects only in parotid glands symptoms may begin in one gland 75 in both obstructions of ducts retards flow of saliva skin over ducts becomes taut and shiny painful when touched mumps slide MC 2800 complications in children rare in adult males may cause orchitis swelling of testes with some damage to reproductive tissue may reduce sperm count 25 of cases in postpubic males develop into orchitis vaccine attenuated virus MMR incidence 400 cases in 1999 RESPIRATORYINFECTION GERMAN MEASLESRUBELLA GERMAN MEASLES RUBELLA family Togaviridae RNA icosahedral envelope with hemagglutinin spikes transmission droplet or contact symptoms mild occasional fever variable pale pink maculopapular rash face gt trunk and extremities rubella rash slide JMC rash develops within a day and fades after another two days mild cold symptoms and swollen lymph nodes possible recovery prompt but relapses possible complications congenital rubella syndrome viruses localize on placenta and pass along umbilical cord destruction of fetal capillaries gt blood insufficiency cataracts cong rubella eye slide MC ST69031 13A glaucoma deafness heart bone and neurological defects stillbirth 50 probability of defects if contracted in first month RESPIRATORY INFECTION GERMAN MEASLES RUBELLA vaccine attenuated virus MMR women should avoid pregnancy for three months following vaccine incidence 260 cases in 1999 MICROORGANISMS AS PARASITIC AGENTS GENERAL PROPERTIES NOMENCLATURE Carolus Linnaeus Sweden 1735 wrote Systema Naturae put plant and animal forms into one classification scheme binomial system name consists of the genus and the species modifier 1 first letter of the genus should be capitalized 2 entire name should be italicized or underlined genus Escherichia or Escherichia species Escherichia coli Escherichia g abbreviated as E coli orig SIZE RELATIONSHIPS size overhead MK9 PHYLOGENY eukaryote from eu true and karyon nut referring to nucleus plants and animals but also protozoa fungi unicellular algae prokaryote from pro primitive and karyon referring to nucleoid bacteria rickettsiae cyanobacteria bacterial cell structure slide JMC eukaryotic cell structure overhead MK 3 MICROORGANISMS AS PARASITIC AGENTS PHYLOGENY further distinctions organelles membranebound compartments where cellular functions occur mitochondria chloroplasts prokaryotic descendant Golgi bodies lysosomes endoplasmic reticulum ribosomes RNAprotein bodies that synthesize proteins symbiosis fusion of primitive cells eukaryotic cell origin overhead MK 8 bacteria became mitochondria cyanobacteria became chloroplasts E UKARYOTES PROTOZOA SURVEY OF PROTOZOA protozoa singlecelled organisms first animals thousands of species exist 2 dozen cause disease of importance third world diseases malaria and sleeping sickness P falciparum slide JMC T brucei slide JMC diarrheal diseases giardiasis amebiasis cryptosporidiosis E histolytica slide JMC G lambia SEM slide JMC diseases of the immunocompromized toxoplasmosis and cryptosporidiosis CHARACTERISTICS OF PROTOZOA eukaryotic morphology size varies greatly generally among the smallest eukaryotic cells unicellular mostly spherical or ellipsoidal trophozoite feeding form cytoplasm enclosed by plasma membrane m cell wall cyst dormant form cell wall protects against adverse conditions EUKARYOTES PROTOZOA classified by means of locomotion flagella cilia pseudopods habitat most are freeliving in moist environments some are parasitic in plants or animals others are symbiotic importance basic part of food chains and webs especially in aquatic habitats zooplankton major cause of infectious disease in humans and other animals EUKARYOTES FUNGI SURVEY OF FUNGI eukaryotic yeasts unicellular about the size of large bacteria yeast slide JMC fermentation of wine and beer bread production molds chains of cells often as a fuzzy mat hyphae slide JMC sporangiophore slide JMC conidiophore slide JMC diseases such as athlete39s foot ringworm and thrush yeast CHARACTERISTICS OF FUNGI morphology cells small 15 pm mycelia visible to naked eye mycelial moldsmulticellular yeast unicellular may be dimorphic yeast gt mold cell walls spore dormant form protects against adverse conditions habitat generally prefer dark moist habitats containing organic material importance mostly saprobes decomposers some pathogens MICROORGANISMS AS PARASITIC AGENTS BACTERIA SURVEY OF PRO KARYOTES Rods bacillus bacilli streptobacilli chain of rods0520 um Spheres coccus cocci sarcina bundle of spheres 05 pm Spirals vibrios spirilla spirochetes Inclusions intracellular bodies 3gtAgtsogtb 10er bacilli E coli bacillus slide MB86 bacilli with spores C tetani EM slide JMC clubshaped bacilli C diphtheriae slide M8145 streptobacilli B subtilis streptobacilli slide M837 diplococci Str pneumoniae diplococci slide M8201 diplococci N gonorrhoeae diplococci slide M828 streptococci Str faecalis streptococci slide M881 sarcinae Sarcina slide MB7 staphylococci S aureus grape clusters slide MB 1 vibrios Vibrio cholera slide M8108 spirilla Spirilla slide M8112 spirochetes T pallidum spirochete slide JMC rickettsia Chlamydia slide JMC FLAG ELLA PILI locomotion for many species 1020 pm long 02 pm thick flagella overhead MKK23 flagella rotate in eukaryotes they whip results in corkscrew motion of flagellum S typhosa SEM of agella and pili slide JMC pilus singular appear as short flagella function 1 in exchange of genetic material conjugation 2 in attachment to surfaces called fimbriae BACTERIA STRUCTURES can enhance ability to cause disease a virulence factor made of protein can act as antigen antibodies can be made against them found primarily on Gram negative organisms N gonorrhoeae important avenue of research develop antibodies to prevent pili attachment of N gonorrhoeae CAPSULE bacterial cell with capsule EM overhead a secreted layer of polysaccharides sugar polymers and small proteins sticky and gelatinous Klebsiella capsule stain JMC Klebsiella culture JMC found on certain cocci and bacilli several functions buffer between cell and environment protects against dehydration prevents nutrients from flowing away prevents phagocytosis by WBCs eg Streptococcus pneumoniae is deadly while encapsulated but harmless with capsule removed virulence factor can attach bacterium to tissue eg Streptococcus mutans dental caries plaque slide JMC attaches to teeth with dextran formed from sucrose bacteria accumulate metabolic breakdown of carbohydrates to acids gt dissolve enamel BACTERIA STRUCTURES CELL WALL all have peptidoglycan except mycoplasmas cell wall layers overhead MKK22 S aureus amp E coli gram stain slide JMC two forms Gram positive larger 25 nm Gram negative smaller 3 nm may relate to gram staining characteristics also have lipopolysaccharide layer endotoxin LPS lipid and polysaccharide may provide protection against antibiotics salts and dyes holds cell together one large molecule protects from bursting from internal pressure penicillin prevents new wall from forming bacteria elongated and burst lysozyme enzyme in tears and saliva attacks linkages between carbohydrate moieties cell wall breaks down and cells explode E coli thin section showing cell wall cell membrane and nucleoid slide JMC BACTERIA STRUCTURES CELL MEMBRANE PLASMA MEMBRANE boundary layer of cell located inside cell wall functions 1 transport of nutrients in waste out 2 energy production composition 60 protein 40 lipid mainly phospholipid arranged as a lipid bilayer one layer outside one inside arrangement fluid mosaic model uid mosaic overhead MKK7 some inside some outside some span membrane dissolving of lipid bilayer leads to cell death by detergents ethanol and certain antibiotics CYTOPLASM intracellular fluid containing proteins carbohydrates lipids nucleic acids salts ions etc ribosomes protein synthesis storage granules chromosome closed loop of DNA suspended in cytoplasm without covering or associated protein nucleoid refers to chromosomal region plasmids extrachromosomal DNA BACTERIA STRUCTURES can carry drug resistance traits R factors can be transferred from cell to cell species to species useful in genetic engineering SPORES endospores highly resistant structures withstand boiling water for two hours 70 alcohol for 20 years radiation humans500 REM sporesmillion REM resist dryingrecovered from mummies longlivedrecovered from sediment gt 7000 years old examples Closz ridium and Bacillus bestknown Bacillus cereus EM spore slide JMC B anthrasis spore stain slide BL25 spore formation sporeformation overhead MKK24 1 DNA replicates surrounded by little cytoplasm and cell membrane coat materials including peptidoglycan additional coats remaining cell disintegrates free spore under appropriate conditions spore germinates liberating bacterium mNOUO IPOON BACTERIA STRUCTURES diseases of interest Anthrax Bacillus anthrasis remain alive in soil periodic reoccurrence the diseases produced by Closz ridium spp require anaerobic environment for spores to germinate Botulism Closz ridium botuinum vacuumpacked can spores germinate make toxin Gas gangrene Clostridium perfringens dead tissue in wound make toxins Tetanus Closz ridium tetani dead tissue in wound make toxin BACTERIA REPRODUCTION AND GROWTH BACTERIAL REPRODUCTION AND GROWTH reproduce by binary fission 1 chromosome duplicates 2 cell elongates 3 plasma membrane pinches inward 4 cell wall thickens and grows inward septum generation EM slide JMC generation time time from one division to the next can be short or long Staphylococcus aureus 30 minutes Mycobacterium tuberculosis 18 hours Treponema pallidum 33 hours Escherichia coli 20 minutes logarithmic growth cell number doubles every 20 minutes starting with one organism in 10 hours at optimum conditions there would be 1073741824 BACTERIAL GROWTH CURVE bacterial growth curve overhead MKK27 lag phase intense metabolic activity acquire nutrients synthesize enzymes prepare for binary fission in host WBCs may engulf some but is balanced by early division BACTERIA REPRODUCTION AND GROWTH log phase reproduction begins gt number of bacteria doubles each generation time in disease symptoms often begin during log growth tissue damage cough fever reactions to toxins stationary phase scarcity of nutrients waste product accumulation reproductive and death rates reach equilibrium effective immune response antibiotic therapy some form spores decline phase number of dying cells exceeds number of new cells host eliminates pathogen TEMPERATURE 3 categories dependent on temperature at which bacteria grow best temperature overhead MKK29 psychrophiles 0 C 20 C mesophiles 20 C 40 C thermophiles 40 C 90 C most diseasecausing bacteria grow between 35 C and 40 C little effect of fever 40 C 104 F on bacteria psychrotrophic coldeating grow at refrigerator temperatures staphylococci on cold cuts leftovers salads can deposit toxins gt food poisoning streptococci can sour milk Proteus vulgaris blacken eggs characteristic rotten odor BACTERIA REPRODUCTION AND GROWTH OXYGEN oxygen requirement overhead MKK32 aerobic require plentiful supply of oxygen anaerobic must have oxygenfree environment some use sulfur in chemistry instead of oxygen make H28 instead of H20 others make methane swamp gas Clostridium examples facultative organisms grow in presence or absence of oxygen many strep staph intestinal rods Bacillus E coli microaerophilic preferjust a little oxygen examples cause disease of oral cavity urinary tract and GI tract BACTERIAL GROWTH MEDIA nutrient broth water beef extract peptone nutrient agar nutrient broth plus agar polysaccharide derived from a marine algae enriched media culture isolation of Staph slide BL20 blood agar nutrient agar plus blood streptococci chocolate agar heated blood agar releases hemoglobin turns brown color Neisseria BACTERIA REPRODUCTION AND GROWTH selective media contain ingredients which inhibit certain bacteria while encouraging others to grow mannitol salt agar mannitol used by staphylococci high salt concentration inhibits most other bacteria eosin methylene blue EMB agar has carbohydrates fermented by gram negatives the dyes inhibit gram positives differential media has ingredients which allow differentiation of various colonies MacConkey agar contains neutral red and crystal violet dyes and lactose bacteria that ferment lactose take up the dyes and turn red bile salts to inhibit gram positive bacteria both selective and differential living tissue culture medium Rickez tsia and Chlamydia require live cells for replication fertilized eggs tissue cultures animals MICROORGANISMS AS PARASITIC AGENTS VIRUSES VIROLOGY HISTORICAL PERSPECTIVE 1892 lwanowski studied tobacco mosaic disease used porcelain filter capable of trapping the smallest bacteria filtered crushed afflicted leaves infectious agent passed through filter reported that a filterable virus was the agent of disease soon others found filterable viruses as agents of specific diseases early 1900 s viruses that infect bacteria were discovered termed bacteriophage 1930 s nucleic acid and protein nature of viruses was discovered Woodruff and Goodpasture fertilized chick embryos used for animal virus propagation living analog of Koch s nutrient agar Stanley virus could be crystallized insight into their simplicity began debate regarding living nature of viruses lifeless similar to crystalline chemical molecule vs living replicates induced fevers stimulates antibody production not associated with chemical molecules 1940 s two significant developments electron microscope allowed visualization of viruses tissue culture Enders Weller and Robbins VIRUSES SURVEY SURVEY OF VIRUSES responsible for many human diseases including influenza hepatitis polio rabies chickenpox AIDS Other viruses slide JMC mycobacteriaphage vaccinia polio adenovirus tomato bushy stunt virus NOMENCLATURE AND CLASSIFICATION widely accepted system has not yet been devised gt lack formal names named after the disease measles the tissue adenovirus the locale of original isolation Coxsackievirus the researcher EpsteinBarr CHARACTERISTICS OF VIRUSES neither prokaryotes or eukaryote microbiologists question whether viruses are living organisms at all noncellular no growth no nutritional patterns no activity except replication exclusively within cells considered to be at the threshold of life structure nucleic acid RNA or DNA surrounded by a protein sheath In uenza schematic slide JMC In uenza TEM slide JMC importance major diseasecausing agents VRUSES STRUCTURE THE STRUCTURE OF VIRUSES size among the smallest agents capable of causing disease 20250 nm in size shape virus shape overhead MKK92 MKK93 helix rabies and TMV icosahedron herpes simplex and polio complex combinations of helical and icosahedral symmetry components virus component overhead MKK91 genome nucleic acid core DNA or RNA not both capsid protein coat capsomeres are subunits provides resistance to temperature pH environment may assist penetration stimulates immune system nucleocapsid genome plus capsid envelope lipidprotein surrounding membrane acquired from host during replication modified by virus may contain spikes which assist in attachment influenza virion completely assembled extracellular virus VIRUSES REPLICATION REPLICATION OF ANIMAL VIRUSES animal virus replication overhead MKK94 attachment specific binding of virus surface or spikes to receptor on cell membrane penetration enveloped virus fuse membranes nonenveloped virus may be phagocytosed uncoating enzymes may strip away capsid or uncoating enzyme is synthesized by host cell using viral coding synthesis and replication new NA and protein components are synthesized maturation and assembly accumulated NA and coat proteins assembled into new virus release by lysis or budding enveloped virus acquire envelope as the exit the cell nonenveloped virus lyse the cell LYSOGENY some infections do not result in lysis temperate virus nonmultiplying virus genome is called prophage or provirus may integrate into chromosome or be carried as a plasmid VIRUSES DETECTION DETECTION OF VIRUSES must provide some form of living tissue easy with bacteriophages use of fertilized eggs Herpes simplex pock formation slide JMC use of tissue cultures viruses are inoculated onto tissue culture monolayer deterioration of cells occurs cytopathic effect CPE cytopathic effect slides l and II JMC detection of antibodies production of visible signs in cells or on body cytomegalic inclusion slide JMC electron microscopy plaque formation bacteriophage


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