Study Guide for Exam 2
Study Guide for Exam 2 SPHU 1020
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This 21 page Study Guide was uploaded by Eleni McGee on Wednesday October 28, 2015. The Study Guide belongs to SPHU 1020 at Tulane University taught by Dickey-Cropley, Lorelei in Summer 2015. Since its upload, it has received 122 views. For similar materials see Cell, Individual & The Community in Public Health at Tulane University.
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Date Created: 10/28/15
Eleni McGee SPHU 1020 02 STUDY GUIDE FOR EXAM 2 Lectures 8 16 Lecture 8 Introduction to Microbiology Key Concepts 0 Bacteria Fungi and Protozoa Viruses Bacterial Classi cation by Phenotype and Genotype Classifying bacteria based on morphology Gram stain External structures of bacteria Classifying Infectious Diseases Going in depth Microbes organisms that are too small to be seen with the naked eye and usually visualized by microscopy Categories Bacteria prokaryote Protozoa eukaryote Fungi eukaryote Medical microbioloqv study of diseasecausing organisms host response to infection diagnosis treatment and prevention of microbial diseases Viruses NOT cells 0 A set of genes packaged in a protein coat either from RNA or DNA Intracellular organism because they must replicate inside a host cell 0 They can move between different bacterial strains ie they can move genes from one strain to another Bacteriophage viruses that infect bacteria 0 Examples of viral pathogens RNA viruses rotavirus causes diarrhea in infants hepatitis A and C HIV rabies OR DNA viruses herpes hepatitis B E ukaryotic Cells Eukaryotes have a nucleus with membrane bound organelles mitotic division and multiple chromosomes 1Fungi a Yeasts and molds lamentous b Mostly free living c Eukaryotic cell structure but with a cell wall 2 Protozoa a SINGLE CELLED parasites b Mostly free living c Sexual or asexual reproduction d Ex Plasmodium malaria or giardia lambia giardiasis Prokaryotic Cells Prokaryotic cells have no nucleus or membrane bound organelles they reproduce by binary ssion Ex Bacteria the smallest living cell some have plasmids circular DNA NOTE plasmids can move from one bacteria to another and transfer antibiotic resistance Bacterial Classi cation 1 Ways to Classify by Phenotype a Gram stain b Observe culture characteristics hemolysis pigment Biotyping based on biochemical reactions Serotyping based on antibodyantigen reactions commercially available e Antibiogram based on pattern of antibiotic susceptibility f Phage typing dif cult outdated 2 Ways to Classify by Genotype more accurate a Nucleic acid based methods can be used for quick ID and molecular ngerprinting methods Qn Writing bacteria s names Classify into genus and species Ex E coli Morphology 1 Arrangement a Usually single or arranged in chainspairsclusters 2 Special Structures a Flagella capsules pili spores 3 Staining a Gram stain i Gram positivepurple ii Gram negativepink b Acid fast stain i Acid fast pink ii Non acid fastbuegreen Classifying bacteria based on morphology 1 Cocci spherical shape 2 Bacilli rod shaped or elongated coccobacilli are short rod shaped 3 Spirochaetes spiraled or coiled 4 Vibrios curved or comma shaped Gram staining process This is the most important stain but you can not use it on mycobacteria use acid fast instead First send a specimen from blood urine phlegm etc to a lab so you can get it gramstained 1 Crystal violet stain 1 min 2 Grams lodine 1 min 3 Decolorize with alcohol or acetone less than 10 secs 4 Counterstain with safranin 30 secs Wash with running water after every step After you stain it you look under a microscope to see if you can identify bacteria in order to give the appropriate antibody lPrinciple of gram stain G will hold onto the stain throughout the process 6 will lose the stain after the process Gram stain gets you a quick diagnosis After a gram stain you can do a culture of the bacteria Bacterial classi cation based on Gram staining 1 Cocci a Gram positive cocci GPC and gram negative cocci GNC 2 Bacilli a GPBGPR and GNBGNR 3 Spirochaetes a Special stains microscopy Rickettsia obligate intracellular gram negative rods produce a distinct category of disease endemic and epidemic typhus Rocky Mountain spotted fever although they are classi ed as bacteria they behave more like viruses Bacterial structure and function Bacterial External Structure MUST KNOW Flagella long coiled structures made up of agellin protein that allow the bacteria to move Because it is made of a protein that protein could be antigenic o Fimbria pili made of pilin protein thinner and more numerous than agella function as adherence factores for the transfer of genes between bacteria Attach to cells to cause disease Capsular polysaccharide capsule is made of polysaccharide visualized by India ink technique promotes adherence to host cell surfaces and to other bacteria Capsules make bacteria more virulent but is poorly antigenic Normal ora bacteria present on human surfaces also known as commensals Sporing stage This occurs when bacteria encounter a harsh environment They go into a quotstate of hibernationquot but can still cause a disease Medical importance of this is that they are resitant to heat radiation desiccation and disinfection They are metabolically inactive they can become vegetative once in the body Detection of microbes 1 Microscopes a Light b Darkfield used for spirochaetes because they don t stain c Fluorescent d Electron 2 Culture a Agar tissue culture when bacteria grow within cells automated systems 3 Antigen detection 4 Antibody detection by serology a Detection of antibodies in blood for example 5 Nucleic acid detection a PCR DNA probes etc Infectious Disease Agents bacteria viruses protozoa protists fungi Helminths animals NOT microscopic U39lbUUNH Incuabation period from time when agent enters body to time of rst symptom Opportunistic infection an infection caused by an organism that is not pathogenic to people with a normal immune system but can cause disease in people with immunosuppression Notes lgG is the most abundant immunoglobulin lgM is the most speci c so that you can detect whether the disease is acute or if the immune response is leftover Classifying Infectious Diseases 1 By duration a Acute b Chronic c Latent periods of no symptoms between phases of illness 2 By location a Local con ned to speci c areas of body b Systemic generalized illness that infects most of body with pathogens distributed by tissues 3 By timing a Primary initial infection in a previously healthy person b Secondary infection that occurs in a person weakened by a primary infection Microbes are ubiquitous in the environment found in humans and animals colonizing our skin and GI tract and more found in commensals normal ora and potential pathogens and nally found in infections and disease Lecture 9 Host Pathogen Interactions Key Concepts Symbiosis Koch s postulates Chain of Disease Transmission In vasion and Toxin Production Neurotoxins Immune Evasion 0 Going in depth Outcome of host pathogen interactions is determined by 1 virulence of organism 2 site of exposure 3 host s ability to respond to the organism Symbiosis living together 1 Mutualism both members bene t 2 Commensalism there is no apparent bene t or harm to either member Ex Normal ora 3 Parasitism one member of the association lives at the expense of the other NOT ALL BACTERIA ARE BAD Help us digest food produce vitamins occupy niches that would otherwise be available for invading pathogens Colonization resistance Probiotics lactobacilli Bacteria in saliva Found in cecum and mouth Koch39s postulates prove a particular organism is the cause of a particular disease 1 The organism should be found in all cases of disease and present in lesions of the disease 2 The organism should be grown in pure culture on arti cial media 3 The inoculation infect experimental animalhuman of the pure culture should result in a similar disease 4 It should be possible to recover the agent from the lesions of the experimental disease Possible issues what if you can t isolate an organisms some organisms are only known by DNA Chain of infection Agent reservoir portal of exit mode of transmission portal of entry susceptible host Epidemiological triad Agent Host Environment Pathogen virusbacteriumparasitefungus Reservoir a place where the pathogen lives and multiplies Animate Rats are reservoir for plague lnanimate contaminated water food etc Mechanism of transmission how the pathogen travels from one host to another or from reservoir to host Susceptible host usually nonimmune or partially immune Carrier hosts carriersl do not show any outward signs or symptoms of a disease but are still capable of transmitting the disease Transmission of infection Mechanisms 1 Spores produced by bacteria and fungi are resistant to dying and will remain in environment 2 Grampositive organisms are well adapted to surviving on skin surfaces such as hands 3 Gramnegative organisms are well adapted to surviving in uids 4 Salmonella and Shigella thrive under conditions of poor hygiene and are transmitted by fecaloral spread 5 More fragile organisms like the one that causes ghonorrea require sexual transmission SKIN is usually a protective barrier Breaks in integrity increase chance of infection MUCOSAL SURFACES ie the gut and respiratory tracts have proteoytic enzymes antibodies and high turnover of surface cells Alterations in mucus distribution cause effects Ex In a smoker the cilia which are hair like projections that push forward foreign particles by coughing are blunted Note bacteria is resistant to lgA proteases 2 Mechanisms of Disease Production by Bacteria 1 Invasion 2 Toxin Pathogenicity ability to cause disease Virulencedegree of pathogenicity Virulence determinants allow a bacterium to produce a disease Bacterial parasites have virulence determinants that allow it to resist the defenses of the host People with strong immunes systems can fend off pathogens better While people with weakened immune systems are more vulnerable to the support and reproduction of pathogens Determinants of Virulence in Bacteria 1 single determinant every time you are infected the disease looks the same a Produce disease by toxin production b Have hardly any invasive characteristics c Depends on a single gene in the bacteria 2 Multiple determinants cause multiple diseasessymptoms a More complete range of diseases in different tissues in the host Bacterial Toxins Exotoxins secreted outside the cell mostly in G bacteria most genes for exotoxins are on plasmids or phages Types cytotoxins kill cells neutrotoxins interfere with normal nerve impulses enterotoxins effect cells lining the GI tract Bacterial exotoxins Mechanisms Extracellular toxins that act on surface Bind to certain receptors or form pores on the cytoplasmic membrane Extracellular toxins that need to enter cell AB toxins diphtheria toxins anthrax toxins cholera toxins Toxins directly delivered into host cell Endotoxins bound to cell membrane usually in G bacteria very powerful toxins cause GN septicemia shock Neurotoxins tetanus o gram spore forming anaerobic rod 0 acts on nerves resulting in inhibition of muscle relaxation o tetanospsmin quotlock jawquot or spasms Botulism o Gram spore forming anaerobic rod 0 Works at neuromuscular junction 0 Prevents impulse from nerve cell to muscle cell 0 Results in muscle paralysis Immune Evasion Capsule loosely structured network usually polysaccharide o Antiphagocytic o Decreased cell lysis o Mimic host polysaccharides Enzymes to destroy leukocytes and macrophages HIV actually infects and destroys cell of immune system Steal iron from hostcarrier proteins Rapid antigenic variation to evade immune response Intracellular pathogens survive within phagocytic cells by inhibiting lysosome fusion with phagocytic cell or escape before lysosome fusion So outcome of infection is balance between pathogen s virulence host immune integrity and response pathogen s ability to evade immune response medical intervention Lecture 10 HIV and AIDS Key Concepts 0 Transmission of HIV HlVbioogy Stages of HIV Infection AIDS quotWindow period Epidemiology and Control STDHI V interaction Going in depth HIV immunode ciency retrovirus has types 1 and 2 but type 1 is most common that results in AIDS It is transmitted through sexual contact contaminated needles mother to child breastfeed in utero delivery blood transfusions health care workers being exposed Of a zoonotic origin HIV 1 common chimpanzee HIV 2 sooty mangabey Almost 50 transmission is male to male sex Discovered 1983 controversial Subtypes HIV type 1 M main and O outlier M classi ed into 10 subtypes A through HIV 1 subtype B Europe and the Americas HIV 1 subtype C SubSaharan Africa most common Infection is aided by Langerhans cells in mucosal epithelial surfaces and aided by presence of other STDs that can produce mucosal ulceration and in ammation CD4 Tlymphocytes have surface receptors which contain follicular dendritic cells that can become infected and provide a reservoir for infecting more CD4 cells HIV binds to cell surface receptors and inserts its RNA which then reverses into DNA Natural history of disease CD4 T4 cells become infected but the disease migrates to other cell types as well Stages 0 Acute infection fever pains lymph nodes enlarge sore throat o Immune response kicks in and virus level stays low for a long time 0 Clinical latency because of immune response person looks heath 0 Loss of CD4 cells and suppression of the immune response 0 Onset of AIDS the cells that respond to HIV infection CD4 are the same ones that the HIV infects and destroys AIDS immunodepression results in opportunistic infections high viral loads and low CD4 counts more virus more CD4 infected and destroyed most people with HIV develop AIDS AIDS de nition CD4lt 200 OR presence of opportunistic infection HIV test HIV Lab testing quotwindow periodquot where it is not detected vefore antibodies appear In this stage you should look for Rna of a virus by PCR This is why you have to return multiple times Rapid tests good because more people to come Strategies to control HIV 1 chemotherapy 2 education 3 barrier methods condoms microbicides gel applied before sex that kills HIV 4 vaccine we don t have one yet STATS Prevalence in adults 34 m Prevalence in children 34 m Incidence adults 27 m Incidence children 18 m Prevention controltreat STDs promote barrier methods prevent vertical transmission blood bank screening needle exchange programs high risk group counseling and testing contact tracingpartner noti cation FP P FP NI STDs increase your risk of getting HIV and giving it to someone else Lecture 11 Tuberculosis Key Concepts 0 Spread of TB 0 Probability of transmission 0 Pathogenesis of TB TB infection vs disease Stages of Diseases Primary infection LTBI and post primary TB Clinical features of TB TB immunity Diagnosing TB MDRTB HIV and TB TB resurgence in the U5 and controlling issues Going in depth Tuberculosis communicable disease caused by the bacterium Myobacterium tuberculosis It is usually chronic Transmission is through tiny airborne molecules called droplet nuclei They are expelled by another person who has infectious TB They can remain suspended in the air for several hours a waxy coat prevents them from rapid dehydration It is most common in developing countries Note Alexander Fleming discovered the rst antibiotic penicillin in 1929 In 1950 the antibiotic for TB was discovered Probability of transmission 1 Infectiousness of the index case TB is more infectious if it is pulmonary TB Infectiousness also depends on whether or not you are getting treatment the type of lesion in lung and how many bacteria or droplet nuclei you cough out 2 Environment insidehigher likelihood of transmission using ventilation to decrease transmission this is why it is likely to get TB on airplanes because enclosed space and low ventilation 3 Duration of exposure Open case someone is actively spreading TB but not on treatment An open case infects 12 to 15 people per year IMPORTANT TB INFECTION IS NOT THE SAME AS TB DISEASE It can infect you anywhere But some common sites Pleura membrane of lungs Lungs Central nervous system Lymphatic system Bones and joints Genitourinary systems disseminated Asymptomatic infection only evidence of infection is a positive TB skin test Pathogenesis of TB Inhaled bacilli may reach alveoli of lungs where they are ingested by macrophages Infection begins when these bacilli multiply in alveolar macrophages Spread through blood stream However most of the time this infection is kept in check by immune system and development of disease is prevented Risk of progression of disease 1 once infected a person stays infected for years maybe for life 2 Risk of disease is 10 per lifetime for HIV negatives and increases to 10 per year for HIV positives Stages of disease 1 primary infection may result in formation of a quotprimary complexquot which is lymph nodes seen in X ray swelling and Ghon focus you can also see a Ghon focus in an X ray towards the top of the lungs a 90 go into latent infection b 10 get disease Latent TB this is why we do a skin test Post primary TB by reactivation or reinfection a Occurs after latent period of months or years after primary infection usually in the lungs Causes lung destruction cavity formation and positive sputum smear JUN Granulomas often in the lungs allow you to diagnose the disease l The central necrosis of the granuloma looks like melted cheese So If positive skin test and no symptoms you have latent TB If positive skin test and symptoms you have TB disease Positive sputum phlegm smear means a person is more infectious In most adults the disease is post primary In children it is mostly primary infection Clinical features Cough Sputum production Weight loss Anorexia tiredness fever night sweats Immunity in TB the pathogen presents a persistent antigenic stimulus There is a loss of blance between cell mediated immunity protective type 1 and pathology Granuloma caviation caseous quotcheesyquot necrosis are all manifestations in lung pathology The agent Myobacterium tuberculosis doesn t stain with gram so acid fast is necessary Pinkpositive You need a contrast to see it better Tests for TB chest Xray clinical exam PPD skin test sputum smear culture for mycobacteria takes a long time and may be negative rapid diagnosis by molecular techniques The Gene Xpert is the most promising new diagnostic test that is based on PCR Treatment of TB and Drug Resistance lsoniazid and rifampicin most powerful bactericidal drugs of the rst line drugs Multi Drug Resistant TB MDRTB By de nition always resistant to INH and refiampicin WHO estimates that 13 of the population is infected with TB doesn t mean that they have the disease TB has had a resurgence in the USD increased 20 between 1985 and 1992 REASONS 1 HIV epidemic 2 Immigration of people who come from areas with high TB prevalence 3 Transmission of B in high risk environments hospitals correctional facilities homeless shelters nursing homes 4 Deterioration of the TB public health care infrastructure DOTS strategy directly observed therapy someone trustworthy observes people taking pill ISSUES IN TB CONTROL HIV MDRTB XDR XXDR no new drug in more than 40 yrs no effective vaccine except for BCG controversial efficacy HIV and TB HIV is a major risk factor for TB HIV reactivates latent TB HIV increases risk of rapid progression to disease after infection Lifetime risk of HIV 10lifetime Risk of HIV 10 year Lecture 12 Food and Watermrne Diseases Diarrheal Diseases Key Concepts 0 Transmission fecaloral foodborne waterborne Classifying diarrhea Pathogenesis by in vasion Pathogenesis by toxin Osmotic in ammatory and secretory diarrhea Cholera Treatment prevention and control Going in depth Diarrhea preventable and treatable It is the leading cause of death in children under ve It is the passage of three or more liquid stools per day or more than normal for a person Generally fecaloral transmission sometimes through water or foodborne Classifying diarrhea 1 By clinical presenation goom e Diarrhea Dysentery blood and mucus in stool foodpoisoning gastro enteritis infame of mucus membrane in stomach and small intenstine enero colitis in ame of mucus membrane in small and large intenstine 2 By Duration a b acute 12 weeks i usually infectious food poisoning parasitic infections viral gastroenteritis ii but non infectious is druginduced or chemical chronic more than 2 weeks i Irritable bowel syndrome ii Colon cancer iii Malabsorption iv Post infectious diarrhea v In ammatory bowel disease 3 By organism a Bacterial viral parasitic 4 By route of transmission a b Waterborne think of Haiti example i Microbes in water ii Common pathogens shigella giardia cholera cryptosporidium resistant to chlorine Foodborne i most common salmonella campylobacter normal ora of poultry Ecoli c Both 5 By mechanism of pathogenesis THIS is the most IMPORTANT one to know a Osmotic diarrhea non infectious b In ammatory diarrhea c Secretory diarrhea People at higher risk older adults young kids the rotavirus is the leading cause of diarrhea in children younger than 2 pregnant women people with weaker immune systems DEFENSE 1 gut mucosa specialized lter acid in stomach peristalsis 2 gut normal ora and protective mechanisms Mechanism of pathogenesis BY INVASION Super cial in ammatory lesion gt fever ab pain dysentery shigella campylobacter Deeper penetration is worse salmonella Mechanism of pathogenesis BY TOXIN PRODUCTION Exotoxins o shigellagt bloody diarrhea o E coligt in ammatory diarrhea Diarrhea classi ed by mechanism of pathogenesis 1 Osmotic Diarrhea a Water is not absorbed in the intestines because of excessive solutes 2 In ammatory Diarrhea a Caused by invasion presence of fever and bloody diarrhea cholera that indicates tissue damage i Shigella campylobacter in poultry salmonella originates in bird intestine amebiasis 3 Secretory Diarrhea a Caused by too much water secretion into the small intestinal lumen b Caused by a noninvasive toxin c Ex Cholera rotavirus More on cholera gram negative rod One A subunit and 5 B subunits A subunit knocks off the normal regulatory mechanism adenyl cyclase keeps producing CAMP so the cascade is kept on causing watery electrolyte rich diarrhea Hydration is key Without intervention it can kill you within 24 hours Treatment usually don t use antibiotics for fear of bacteria developing resistance speci c drugs for protozoa are used Prevention good hygiene protected water supply safe food supply quotboil it cook it peel it or forget itquot Haiti cholera outbreak good example to know Lecture 13 Emerging Infectious Diseases Key Concepts 0 Factors involved in Ele In uenza Ebola Dengue SARS West Nile Bioterrorism Category A B and C agents Going in depth Emerdind infectious diseases Diseases whose incidence in humans has increased in the past two decades or threatens to be increased in the near future Can be new reemerging or drug resistant Important emerging and reemerging diseases HIVAIDS malaria TB in uenza SARS West Nile Marburg bioterrorism Characteristics of Ele 70 are of zoonotic origin most are caused by pathogens already present in the environment that are given a selective advantage with changing conditions like human action or natural causes Factors involved in Emergence of Infectious Diseases KNOW 1 Ecological changes and Agricultural Devleopment a Often associated with zoonoses having high mortality rates b Ex Lyme disease u standing bodies of water result in increase of arthropod vectors leading to outbreaks of dengue West Nile etc 2 Changes in Human Demographics and Behavior a Urbanization b Human behavior can change disease patterns ex STDs HIV c Commercial air travel 3 International Trade and Commerce a Plague trade ships and yellow fever slave trade b Cholera reintroduced into South America by ships from Asia and West Nile in the US 4 Technology and Industry a Inappropriate animal feed i Mad cow disease b Medical technology c Mass food production and globalization of food sources increases impact of contamination i E coli 0157 in hamburgers caused recas in the news 5 Microbial Adaptation and Change a Antibiotic resistance b Mutations and acquisition of new virulence c Microbial adaptations to the host d Antimicrobial resistance 6 Breakdown of public health infrastructure a Closing TB programs slashing budget b Gaps in medical training leading to misdiagnosis c Relaxing immunization policies d New pathogens need new testing methods that aren t yet available Major Ele 1In uenza Keeps changing the HA and NA on the cell membrane It is a single strand of RNA broken into eight segments Seasonal in uenza different than pandemic in uenza Pandemic in uenza ex If pig gets human in uenza and duck in uenza virus it can mix up the RNA of each and create a new virus a completely different antigen e Seasonal u vaccine surveillance centers predict what strains to mix based on what they observe the most of f Antigenic shift due to a major change pandemic entire gene g Antigenic drift small mutations seasonal point mutations goom a Zoonotic mostly likely from bats b Transmitted through blood bodily uids and excreta c Infectious people are not contagious until the onset of symptoms d Pathogenesis i Direct infection of tissues ii Immune dysregulation iii Hypovolemia and vascular collapse e High fatality rates 3 Dengue 4 SARS 5 West Nile Bioterrorism deliberate release of viruses bacteria or other germs used to ause death or illness in people animals or plants ex Antrhax 2001 sending anthrax spores in mail caused nationwide effects concerns and panic Category A Can be easily disseminated or transmitted from person to person and results in high mortality rates Ex Anthrax botulism plague smallpox Category B Moderately easy to disseminate and result in moderate morbidity and low mortality rates Category C Third highest priority that include emerging pathogens that could be used for mass destruction in the future because of availability ease of production and potential Ex Hantavirus nipah virus Prions infectious proteins Lecture 4 VectorBorne Diseases Malaria Key Concepts 0 Disease terminology o Malaria pathogenesis types clinical features life cycle prevention treatment epidemiology Going in depth Agent virus bacteria parasite Vector carries disease to host but does not necessarily get disease usually mosquito Reservoir where disease replicates in nature Control reduced transmission low number of new cases Elimination low transmission no new cases Eradication disease only alive in organisms in lab Endemic constantly present in a certain area Epidemic sudden outbreak of disease con ned within country borders Pandemic sudden outbreak of disease that crosses country borders Know an example of pathogen its vector and a disease transmitted for Virus bacteria protozoa helminth Pathogens Vectors Disease transmitted Virus Mosquito West Nile dengue Bacteria Tick Lyme disease Protozoa Mosquito Malaria Helminths worms Mosquito Filariasis Vector borne disases 1 Mosquitoborne 2 Louseborne 3 Tickborn 4 Miteborn Malaria Basic facts Caused by plasmodium a type of protozoa Season transmission because of mosquito lifecyceany standing water can be breeding ground for mosquito Vector FEMALE anopheles males don t have blood meals because they don t lay eggs Causes 300500 million cases per year worldwide and around 2 million deaths Mortality is primarily in subSaharan Africa among children younger than 5 Endemic area Caused by parasite Plasmodium and transmitted by mosquitos vector No nonhuman reservoir No vaccine No sterile immunity after infection repeated infections possible Dormant stage in some species 2 most important species of malaria 1 Plasmodium vivaX a Most widespread found in most endemic areas including some temperate zones only infects red blood cells 2 Plasmodium falciparum a Primarily tropics and subtropics worse causes the most fatalities more merozoites Malaria is transmitted in nature by mosquito and rarely by birth congenitally or sharing syringes blood transfusions Life cycle of malaria 1 During a blood meal a malariainfected female Anopheles mosquito inoculates sporozoites into the human host Sporozoites infect liver cells and mature into schizonts Schizont collection of merozoites in a red blood cell that can burst at any time 2 After this initial replication in the liver exoerythrocytic schizogony the parasites undergo asexual multiplication in the erythrocytes erythrocytic schizogony Erythorcytic red blood cell cycle Exoervthrocvtic liver cycle 3 Merozoites infect red blood cells The ring stage trophozoites mature into schizonts which rupture releasing merozoites 4 Some parasites differentiate into sexual erythrocytic stages dametocvtes Blood stage parasites are responsible for the clinical manifestations of the disease Important notes Exoerythrocytic and erythrocytic cycles are both asexual Cycles in the vector are erythrocytic At the end of the cycles more sporozoites are made and spread the process is repeated Hypnozoites only in the P vivax and P ovae strains When malaria is in the dormnt stage may not immediately go into schezogeny You can test for malaria by a blood smear Look for red blood cells that are enlarged and lled with merozoites Look for schizonts Immunity Develops slowly Premunition when you have immunity after getting the disease once is short lived No durable immunity Semiimmune adults in endemic areas Pathogenesis ONLY Red blood cell trophozoites and schizonts cause disease NO liver pathology caused by hepatic schizonts or sporozoytes Mechanisms of pathogenesis 0 RBC destruction by parasite immune hemolysis in spleen o Antigenantibody complexes in kidney o Schizonts of P falciparum stick to endothelial cells of blood vessels and cause hypoxia or shock this is cytoadherence This can cause cerebral malarial blockage in brain 0 Cytokines and mediators released causing shock and capillary leakage Clinical features Prodromal symptoms 0 lncubation 14 weeks 0 lntense fever every couple of days 0 Cycles of fever and chills 0 Flu like symptoms Treatment No vaccine Prevention chemoprophylaxis 0 Medication taken at regular intervals 0 Take especially before travel and a few weeks after travel Treatment 0 Clinical cure eradication of RBC trophozoites and schizonts o Radical cure eradication of RBC trophozoites and schizonts and hepatic schizonts dormant Control 0 Prevent transmission Prompt recognition and treatment Prophylaxis for travellers and pregnant Environmental control don t leave out any standing water Mosquito nets Permethrin know this Insecticide treated nets ITN OOOOOO
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