New User Special Price Expires in

Let's log you in.

Sign in with Facebook


Don't have a StudySoup account? Create one here!


Create a StudySoup account

Be part of our community, it's free to join!

Sign up with Facebook


Create your account
By creating an account you agree to StudySoup's terms and conditions and privacy policy

Already have a StudySoup account? Login here


by: Cassie Koepp


Cassie Koepp
GPA 3.61

R. Farrar

Almost Ready


These notes were just uploaded, and will be ready to view shortly.

Purchase these notes here, or revisit this page.

Either way, we'll remind you when they're ready :)

Preview These Notes for FREE

Get a free preview of these Notes, just enter your email below.

Unlock Preview
Unlock Preview

Preview these materials now for free

Why put in your email? Get access to more of this material and other relevant free materials for your school

View Preview

About this Document

R. Farrar
Class Notes
25 ?




Popular in Course

Popular in Biological Sciences

This 126 page Class Notes was uploaded by Cassie Koepp on Tuesday October 13, 2015. The Class Notes belongs to BIOL 4105 at Louisiana State University taught by R. Farrar in Fall. Since its upload, it has received 15 views. For similar materials see /class/222831/biol-4105-louisiana-state-university in Biological Sciences at Louisiana State University.

Popular in Biological Sciences




Report this Material


What is Karma?


Karma is the currency of StudySoup.

You can buy or earn more Karma at anytime and redeem it for class notes, study guides, flashcards, and more!

Date Created: 10/13/15
Parasitisim is a symbiotic relationship Symbiotic relationship 0 Commensalism one gets harmed o Mutualism both benefit 0 Parasitism one benefits parasite and one is harmed host 9 not usually killed 0 Parasite wants to host to be alive Protozoans Helminths and Arthropods Parasitic disease 0 Direct effect parasite itself 0 Indirect effect host defense mechanisms HostParasite Relationship 0 Innate immunity born with and doesn t require prior exposure 0 Acquired born with ability but needs to be activated 0 3 lines of defense 1 First line nonspecific physical barriers 2 Second line nonspecific innate and always quotonquot 3 Third line specific and acquired immune system prior exposure required 1st Line of Defense 0 Skin outer layer of skin cells are mainly filled with waterproof keratin o Mucous membranes 0 Sweat saliva tears 2quotd Line of Defense 0 Used when things have gotten inside the body passed through 151 line of defense 0 WBCs 9 connective tisse o Neutrophils PMNs majority of what is in blood Monocytesmacrophages o Eosinophils o Lymphocytes 0 Natural killer cells derived from lymphocytes 0 Basophils 9 least abundant o Antimicrobialproteins o Inflammatory response How do you differentiate between plasma and serum 0 Serum is plasma with all the particulates removed Neutrophils 9 seek destroy die 0 Major phagocytic cells quotProfessional Phagocytequot 0 First on scene 0 Nonspecific o Nondividing and shortlived 9 go to destroy and die in the process 0 Granules contain hydrolytic enzymes to destroy what they engulf by phagocytosis Macrophages o llProfessional phagocyte o Killersscavengers clean up crew 0 Long lived 0 Can divide on site Eosinophils o Cytotoxic cell 0 Has granules that contain cytoxic toxins o 2 conditions that elevate circulation o Antiparasitic activity 0 Allergic responses Natural Killer Cells 0 Derived from lymphocyte stem cells but play no role in immune response 0 Nonspecific cytoxic 0 When cells are abnormal and have abnormal markers natural killer cells aren t prevented from attacking o Lyse cells 0 Defense against tumor cells and infected cells Antimicrobial Protiens o Nonspecific 0 Some circulate in plasma 0 Complement factors 0 Some released by injured damaged tissues 0 Cytokines Table 32 text Inflammatory Response 0 Nonspecific 0 Only in living organisms 9 antemortem process 0 Always responds to any tissue damage in same way 0 Signs of inflammation 0 Heat 0 Redness o Swelling 0 Pain Tissue Injury not necessarily an infectious response causes an inflammatory response 0 Injured cells release inflammatory mediators 0 Blood vessels first have to dilate 0 Increase blood supply to affected area 9 causes redness and heat 0 Fluid then leaks from vessels and allows migration ofWBCs into tissue 9 swelling 0 Peripheral nerves damaged by injury or irritated by swelling 9 pain Lesion any pathological change in tissue wound bruise rash papule skin spots not specific Pathology abnormal conditions creased as a result of the structural and functional changes caused by the disease process Purulent exudates pus dead neutrophils dead tissue extravascular fluid Abscess pusfilled cavity lesion created by inflammatory process Ulcer lesion that opens to surface Acute inflammation sudden onset 0 Site of tissue injurydamage infection 0 First responders still main cell population at site neutrophils Chronic inflammation ongoing o Stimulation continues causative agent still present 0 Macrophages are not the major cell population Granuloma accumulation ofinflammatory cells p 39 r 0 around39 quot y causative agent 0 Accumulation becomes walled off by fibrous connective tissue isolation the causative agent 3rd Line of Defense 9 Immune System 0 Acquired because requires actiation specific 0 Has memory initial contact will cause recognition for future infections 0 Adaptive improves with each successive encounter Primary Organs of Immune System 0 Bone marrow o Thymus Secondary Organs o Lymphatics nodes and vessels 0 Spleen o Mucosa associated with lymphoid tissues MALT Immune Effector Cells 9 Lymphocytes Vessels structure that conveys a fluid includes blood vessels and lymphatic vessels Lymphatic system does work with the circulatory system not totally separate Antigen Ag any quotforgeignquot not recognized as self not normally found in body molecule that elicits a specific immune response 0 Initiates immune response 0 Driving force of immune response Antibody protein secreted by B cells in response to a speci c antigen Immune Effector Cells primary WBCs involved in immune response 0 Lymphocytes o B cells antibody producers I Has surface Ag receptors called membrane antibodies 2 binding sites I All Ag receptors are identical and specific for same Ag I Ab produces and released is same 0 T cells I Have surface Ag receptors one binding site Structurally similar to receptors on B cells I All receptors are identical and specific for same Ag 39239 Cytotoxic T cells defenders quotkiller cells Helper T cells facilitators activate B and T cells 2 Major Categories of Immune Responses 1 Humoral antibody mediated immunity 0 Can go after extracellular pathogens 0 B cells 2 Cell Mediated o Cytotoxic T cells killer cells 0 Go after intracellular pathogens Immunological Memory o Is induced 0 Primary immune response first contact 0 All other contacts with same antigen is a secondary immune response 0 Occurs as a result of memory cells Clonal Explansion division and differentiation ofT and B cells in response to antigen 0 Results in formation of o B cells I Memory cells sentinals9 long lived remain in circulation I Plasma cells warrior cells 0 T cells occurs with both cytotoxic T cells and helper T cells I Active T cells I Memory T cells Secodnary immune respone happens quicker Development of Self Tolerance 0 Removal of all immune cells with recpotrs capable of reacting with quotselfquot components 0 Process occurs during the maturation process of T cells and B cells 0 Maturation process 0 T cells migrate to Thymus o B cells stay in bone marrow Apoptosis programmed cell death 0 Cell commits suicide 0 Single to cell surface receptor o sUIcIde proteIns In cell actIvated I Proteases I Nucleases o For T and B cells this removes all cells with surface receptors capable of reacting with normal molecules belonging to you 0 Normal development process and is involved with more than the maturation process ofT and B cells How do we recognize quotselfquot and quotnonselfquot 0 Major histocompatibility complex MHC 9 molecules are not antigen specific 0 Components of cell membranes 0 Protein quotselfquot markers 9 biochemical fingerprint 0 Class 1 MHC on all nucleated cells RBCs don t because they don t have a nucleus 0 Class 2 MHC on specialized cells 0 Macrophages o B cells 0 Functions 0 quotselfquot ID tags 9 primarily MHC 1 o Antigen presents to T cells I Present Ag that react with T cell receptors I MHC 1 to cytotoxic T cells I MHC 2 to helper T cells Cytotoxic T cells 0 Recognize Ag presented by MHC 1 molecule 0 Have Ag receptor for specific Ag 0 Have a coreceptor for MHC 1 molecule CD8 Helper Tcells o Recognize Ag presented by MHC 2 molecules 0 Have Ag receptor for specific Ag 0 Have coreceptor for MHC 2 molecule CD4 TH1 activate CMI cell mediated and cytotoxic T cells TH2 activate humoral and B cells Antibody Classes a gM first contact antibody very large b lgG produced in primary response after IgM production can cross the placenta o Anamnestic secondary response antibody c gA secretory antibody usually comes in form of a dimer d gD not essential don t know what it does e gE important in parasitic infections and involved in allergic responses High eosinophils and IgE mean parasitic infection or allergic response Antibody Morphology o Antigen binding site yquot configuration 0 2 Ag binding sites per antibody molecule MHC 2 proteins present Ags to THZ cells Active immunity engaged immunity Passive immunity used when don t have time to wait for active immunity Problems of poverty high population lack of health care sanitation nutrition and education Pinworms enterobius vermicularis number one infection in US Pathogensis process involved in development of disease 9 how Etiology study of cause of disease 9 causative agent name the parasite Infection vs Disease not synonymous E To infect to enter inhabit and reproduce within another organism El Infection organisms entering inhabiting and multiplying in your body El Disease characterized by presence of clinical signssymptoms caused by organism living in your body El Non pathogenic organisms does not cause disease in host El Pathogen can cause disease in host General Characteristics of Protozoa Single celled eukaryotic organisms 1 nucleus as a rule motile most only a small fraction are parasitic in man protozoa gain entry into host 3 ways 0 orally host ingests infective stage 0 vector bites 0 sexual transmission STD Reproduction in Protozoa El general rule asexual in host 0 asexual Ibinary fission one become two 0 multiple fussion one becomes many schizogony Imerogony Elgametogony ametes sexual stage 0 sexual Elfusion of gametes syngamy Dygote D D D D Amoebas and Ciliates Text chapter 7 and chapter 10 pg 176177 volitila coli sp General Characteristics of Amoeba El Morphology o 2 forms DUDE D D D D Eltrophozoite feeding and reproducing forms single cell 1 nucleus with endosomes aka karyosome nucleolus D D Icyst El environmentally resistant form El infective stage for new host Transmission 0 Direct life cycle ICyst ingested by new host INO intermediate host Reproduction o Binary fission Most amoeba on this planet are NOT parasitic Phylum Sarcondina Order amoebida Family Endamoebida El Genus Entamoeba o Endolimax o Lodameba 5 species infect humans 0 E histolyticaljathogen E disparldommensal o E colildommensal o E hartmannildommensal E gingivalisldommensal Lochse in 1875 O O Schaudinn1903 studied E histolytica Entamoeba histol ica D D D D Distribution worldwide morphology 2 stages 0 trophozoite Imotile Iphagocytic El feeds on host cells Ireproduces by binary fission o cyst Iinfective stage Iresistant to environment El survive weeks in moist environment El chlorinationljvont kill it El dry heat or freezing can kill host niche 0 large intestine and rectum transmissionlllirect o ingestion of cyst Elfecal contamination of food and or water contamination via hands El feet of flies cockroaches etc Isexually transmittedljmal sex Severity of Parasitic Disease 0 Depends on Ellmmune status of host and size of infective dose El Clinical ClassificationEAmebiasis o Asymptomaticljisymptomatic Carrier INo clinical signsldyst passers Noninvasive infection El Host defenses helping hold parasite in check Trophozoites rapidly form cysts CIA source of infection for others so it is pathogenic El Shed cysts El Is a pathogenic strain of E histolytica o Symptomatic intestinal amebiasis Acute amebic colitis El Diarrhea aka Amebic colitis o Diarrhea is most common clinical presentation IDiarrhea of more that a few days duration IDefined as semisolid or fluid fecal matter discharged form the bowel El Acute amebic colitis 0 Wide range of presenting symptoms 0 Mild moderate or severe diarrhea o Pathogenesis of amebic colitis IAttaches to surface of mucosal cells of large intestine ILyses cells Invades large intestine tissues feeding on mucosal cells DCan cause characteristic ulcers in gut mucosa Ellf develop deep ulcers then can metastiasize go extraintestinal El Deep ulcers reach blood vessels and lymphatic vessels to start infection in other places besides you GI tract El Dysentery o Amebic dysentery IDysentery bloody mucoid diarrhea The most severe form of amebic colitis El Can be life threatening EITender abdomen Pain cramping El Tenesmus IFever IWeigh loss ITrophozoites in feces IMuch more than blood in feces Ellncludes bleeding into gut lumen with sloughing of gut mucosa Chronic amebic colitis Recurrent bouts of diarrhea but NO dysentery Abdominal pain Trophs and cysts in stool Ulcerations in mucosa that don t erode into blood vessels Can get complications with chronic forms Possible of Chronic Amebiasis o Gut performationljaeritonitis DDDDDD o AmebomaEdImebic granuloma IMass in large intestine DComposed of amoeba trophozoites macrophages eosinophils lymphocytes and necrotic cellular debris DCan be large enough to cause gut obstruction EIFeeds on El Your cells 0 Mucosal cells 0 RBCs o WBCs o Extraintestinalamebiasis Effects of parasitic infections 0 Overt disease 0 Tissue changes 0 Insidious effects 0 O O O O Malnutrition Malaise don t feel good Lethargy 9 anemia Fever Stunted development physically and mentally Hyperplasia normal cell growth at accelerated rate Hypertrophy don t get more cells each cell gets bigger Metaplasia conversion of tissue type into another 0 Not necessarily abnormal 0 May be reversible or convert to neoplasia Neoplasia abnormal cell growth that doesn t respond to normal cell growth factors 0 Malignantneoplasm o Benign neoplasm Zoonosis animal to man only Symbiosis 2 organisms living close to each other Ectoparasites quoton host external Endoparasites quotin hostquot 0 Obligate must live in a host 0 Facultative not normally parasitic but can live as a parasite if enters the body opportunists o ncidental wrong host 0 May not survive 0 May not complete life cycle 0 May not establish infection 0 Or could be highly pathogenic Definitive host harbors sexual stages sexual reproduction occurs in host Intermediate hosts required in life cycle of parasite PAM diagnosis usually postmortem misdiagnosed as bacterial meningitis PAM treatment none specifically o Amphotericin B IV and intrathecal o R Characteristics of PAM 0 Cause Naegleria fowleri thermophile free living 0 Fresh water borne 0 Warm months only 0 Enters through the nose 0 Only find trophozoites in host lesions only in brain 0 Rapid onset and rapidly fatal 57 days 9 acute 0 Equal opportunity agent Definitive diagnosis comes from histopathological diagnosis Acanthamoeba spp 0 Family Hartmanellidae 0 Most common amoeba in soil and water sea water fresh water tap water hot tubs HVAC 0 Multiple entry points 9 eye lesions lungs skin 0 Find both trophs and cysts starshapes like crystals in lesions Clinical Disease 0 CNS 9 GAE o Immunocompromised only 0 Slower progress than PAM can be several weeks in duration till death Clinical signs headaches seizures mental confusion lethargy and coma I No way to differentiate between PAM 0 Fatal Characteristics I Cause Acanthamoeba spp O O I In soil and water ofall kinds salt fresh brackish Any time of year I Entry sites lungs skin I Trophs and cysts in lesions lesions can be outside of CNS I Slower onset several weeks but still fatal 9 chronic compared to PAM 0 Skin Disease 0 Cutaneous entry Acanthamoeba skin plaque o Susceptible individuals 0 Eye 9 ulcerative keratitis 0 Causes a associated with contact lens wear 39239 Cleaning contact lens with nonsterile water 39239 Wearing contacts during water activities b trauma to eye with exposure to contaminated soil or water 39239 Includes noncontact wearers o Corneal infection trophs and custs I Get trapped under contact 0 Clinical signs severe ocular pain blepharospasm squinting and tears conjunctivitis corneal ulcers 0 Keratits is not conjunctivitis 0 Frequently misdiagnosed as viral keratitis I HSV herpes simplex virus Acanthamoeba cysts resistant to o Dehydtartion 0 Temp extremes 0 Most sterilizing agents including chlorine 0 Variety of antimicrobials Treatment 1 Systemic antifungal drug 9 treatment is difficult but untreated leads to blindness 2 Topical antiamebic eye drops 3 Debride necrotic tissue of cornea 4 May require keratplasty corneal transplant Prevention 0 Use only sterile cleaning solutions to wash contacts 0 Don t where contacts in water Balantidium coli 0 Phylum Ciliophora Family Balantidiidae 0 Only ciliate capable of infecting man 0 Worldwide tropical regions 0 Endemic where pigs are a major part of diet 0 Reservoirs pigs commensal in pig o Trops and cysts Infection stage of Balantidium coli cyst o Trophs pass out in feces 9 can encyst outside Balantidium coli DX o Cysts in feces 0 Biopsy of rectum or colon Treatment Tetracycline DDOC binds to tissues undergoing calcification especially unerupted teeth odoquinol Flagyl Not for children younger than 8 0 Not for pregnant women Prevention good hygiene most infections are result of close association with pigs Hemoflagellates Hemoflagellate flagellated protozoan that spends at least one stage of development in host blood Heteroxenous undergo development in at least 2 different hosts Order Trypanosomatida o Trypanosome species 0 Leishmania species 0 Pleomorphic life cycle stages Morphological Forms of Hemoflagellates o Amiastigote intracellulart no flagella or undulating membrane 0 Promastigoteflagella o Epimastigote flagella and small undulating membrane 0 Metacyclic trypomastigote infective stage for vertebrate hosts 0 Trypomastigote found in blood quot 39 long 39 39 39 U 39 and flagella Salivarian transmission all are indistinguishable from each other9 T brucei brucei can t infect humans Tb gambiense Tb rhodesiense Stercorarian transmission 9 T cruzi Salivarian anterior station entrance through vector bite wound by transmission of parasite in vector saliva Stercorarian posterior station entrance through vector bite wound by contamination of bite wound with infected vector feces containing parasite American trypanosomiasis 0 Human African trypanosomiasis HAT o quotsleeping sicknessquot o T brucei gambiense West Africa 0 Tb rhodesiense East Africa 0 African trypanosomiasis o quotnaganaquot o Tb brucei Tsetse fly Glossina spp 0 Fly belt 9 15 N and 25 S latitude in Africa 0 One bite has about 400 metacyclic trypomastigotes Tb rhodesiense and Tb gambiense o Morphologically identical 0 Differe in pathogenicity 0 Different time scale of development of clinical signs Tb gambiense 0 Chronic from of HAT 0 West and central Africa 0 ncubation months to a over a year 0 CNS signs year or more 0 Human 9 Tsetse fly 9 human Tb rhodesiense 0 Acute form of HAT 0 East and central Africa 0 Incubation time weeks 0 CNS signs weeks 0 May be fatal before CNS signs 0 Reservoir wild game African Trypanosome Life Cycle Stages 1 Epimastigote in vector only 2 Metacyclic trypomastigote infective stage 3 Trypomastigote in vertebrate host Additional means of tranismission 0 Blood transfusions from infected human host 0 Eat raw meat from infected animal host 9 Tb rhodesiense only 0 Extremely rare sexual transmission 9 Tb gambiense only HAT Disease Progression 1 Bite reaction chancre o Ulceration at bite site 1 week post infection I Inflammatory response to parasites at site I Parasites stay in interstitial fluid at site until complete transformation to trypomastigote form 0 Transient lesion I After transformation parasites move out and chancre heals within 23 weeks leaving no scar 2 Stage I o Parasitemia waves rise and fall in parasite level in blood I Due to immune system kicking in 0 Systemic febrile illness All of this occurs faster with Tb rhodesiense 3 Stage II 0 causes llmeningoencephalitis these changes indicate that the parasite has made it to the brain I severe headaches I seizures and tremors I still neck I personality change I emaciation somnolenceasleepy 0 when the parasites get into the brain inflammation immune response damage tissue in brain which results in the release prostaglandin D2 will elevate the level of serotonin which is the precursor that activates the production of melatonin in the pineal gland progression to coma Disease results in Death even with treatment Blood brain barrier does not let anything to the brain that is not lipid soluble It keeps things that are in the blood stream from getting easy access to the brain Exception hypothalamus We don t know how the parasite crosses the blood brain barrier What is causing those waves of parasites 0 Your immune system is working like normal but the parasite will jump ahead of your immune system by antigenic variation by parasite 0 Can do this by changing the surface protein coat 0 they are masters at this Variant Surface Glycoprotein VSG o Glycoprotein coat on surface 0 All protein molecules on trypomastigote are identical molecules 0 Most tryps present in blood express same VSGa clones o VSG s are very antigenic 0 Can enzymatically clop of entire glycoprotein coat 0 Express a different VSG gene and produce a new coat with different antigenic determinant 0 Change VSGa change surface antigen 0 With every change you body s immune system has to start from scratch Antigenic Variation in Trypanosomes snwasz Pathogenesis of HAT 1 2 3 Clip off old VSG coat with one specific enzyme Express a new VSG genea never duplicate VSGs Have gt 1000 genes in parasites genome for VSG s No repeats of VSG s in same host No crossreactivity between VSG variations Random pattern of gene expression for VSG s Immune system of host is forced into a new primary response with each VSG change Final outcome without Rx exhaustion of host immune defenseadeath Glucose depletion parasite use 50x greater than host a Lethargy emaciation b Because the glucose made by your body is taken by the parasite and the body is resulting to breaking down fat and proteins for energy Tissue damage in CNS a Inflammation cerebral edemaa coma Exhaustion of immune system a Antigenic variation keeps parasite a jump ahead of host b Eventually lymphoid organs depleted of lymphocytes c Nodes shrink and fibrose Quick Review of Clinical Disease NH 5 P Chancre formation at bite site a disappears Stage I parasitemia and systemic febrile illness a Initially clinical signs are nonspecific Stage II invasion ofCNS a Rare but documented with T gambiense ONLY Transmission a Tsetse fly bitea 1 transmission mode b Blood transfusions c Raw meat from game animals i T rhodesiense only d Sexually transmitted 4 cases in T gambiense ONLY Dx a History of travel in endemic region tsetse fly region b Chancre if still there c Parasite in blood smear CSFa cerebral spinal fluid test d Immunodiagnostic test CA I39I39a Card Agglutination Trypanosome Test 0 Designed to detect specific host antibody to T gambiense 0 Can use whole blood of CSF 0 Host IgM titer high 0 Good agglutinating Ab 0 Must still confirm with finding parasite Pentamidine o Inhibits DNA replication in parasite o Breaks apart circular DNA 0 Cannot get into brain of host so only good for stage I Suramin if not CNS signs 0 Blocks cellular respiration in trypsa enzyme inhibitor of ATP in parasite 0 Cannot get into the brain Melarsoprol arsenical very toxic 0 510 die from treatment 0 damages heart kidneys peripheral nerves brain 0 only drug for T rhodesiense after CNS signs occur stage II 0 recent reportsa resistance developing DFMO difluoromethylornithine resurrection drug 0 99 effective for T gambiense o quotResurrectsquot patient after already showing CNS signs 0 enzyme inhibitor 0 Untreated death T gambiense T rhodesiense Hemolymphatic stage stage I Hemolympahic stage I pentamidine DOC Suramin DOC Suramin Stage II CNS stage Stage II Melarsoprol DFMO African trypanosomiasis o Nagana o Tb brucei only in animals Trypanosoma brucei brucei 0 Not human pathogen 0 Cannot infect humans 0 We have lipoprotein HDL in our plasma called trypanosome lytic factor TLF which lyses the trypomastigotes o Nagana disease of livestock 0 Highly pathogenic in any imported stock cattle camels horses pig goats o Rapidly fatal 0 Native cattle breeds infected but not severely affectedaremember coevolution o Reservoira African ruminants o The Ecological guardian of Africa because new species cannot survive Prevention steps 0 Surveillance and Rx of new cases 0 Fly trapping o Destruction of tsetse habitat o What stopped prevention steps in Africa 0 Poverty 0 Political upheaval 0 Civil unrest I People pushed into tsetse fly regions American Trypanosomiasis o Chagas Disease 0 Trypanosoma cruzi 0 Vector Triatomine insects o Aka kissing bug bc the bite is relatively painless Trypanosoma cruzi Transmission Modes 0 Vector borne o Transplacental 0 Blood transfusions 0 Organ transplants o Immunosuppresants allow dieseas to spread rapidly 0 Oral 0 Eating infected insects 0 Drinks made from sugar cane juices 0 Eating acai palm fruit 0 Feces without bug contact Detailed explanation of triatomine bug life cycle 0 Trypomastigotes control the pH so that the lysosomes can t get activated 0 No antigenic variation 0 Have intracellular stage 0 Can be distinguished by its morphology 0 Host all mammals including mana is a zoonosis 3 Life Cycles o In vector 39 39U and quot u U o In mammalian host u 39U 9 g 9 u U Primary Tissue Niche for T cruzi 1 Mucles cells of hollow organs 9 heart and gut 2 Neuron support cells 3 Also invade bone marrow spleen liver lymph nodes macrophages T cruzi Clinical Disease once infected infected for life 0 Acute Chagas disease 0 Can cross plancenta and infect fetus 0 Child can be born with disease 0 Chronic Chagas disease 0 Can cross placenta and infect fetus Chagoma firm red raised swelling 0 Localized reaction at bite site not an ulcer 0 Transient lasts several weeks will disappear o Romana s sign chagoma of eye swollen eyelid and periorbital edema Acute Chagas Disease 0 Onset 412 DPI 0 Usually illness in children 0 Can be asymptomatic in adults 0 Clinical signs variable in children 0 Fever 0 Myalgia muscle pain 0 Severe anemia O Myocarditis I Tachycardia and arrhythmias I CHF I Progress to cardiomegaly especially in children under 5 Myocarditis inflammation of heart muscle Cardiomyopathy disease of heart muscle Cardiomegaly enlarged heart Pathology 0 Direct damage to cells are destroyed 0 Indirect damage to neurons 0 Pathognomonic lesion characteristic lesion indicative of a particular disease 0 Cardiomegaly heart damage that occurs after myocarditis Pseudocyst in heart muscle Chronic Chagas Disease 0 Survived acute phase 0 May be mild or asymptomatic silent in adult for years long latent period 0 Most beyond small children under 5 o Organisms continue to damage affected organs 9 especially heart 0 Cardiomegaly CHF GI problems 0 Organ damage can cause progression to o Megaesophagus 9 dysphagia o Megacolon o Megabladder and megaureters rare 0 Indirect damage to neurons 0 Lack of innervations 9 lack of muscle tone 9 muscle becomes flaccid and organ enlarges Chronic moms can give birth to acute babies Don t invade neurons but destroy the support cells around the neurons Evasion of Host Responses o Intracellular location 0 Blocks killing mechanisms of infect cells 0 Neutralize pH of vacuole and produce perforinquot protein poking hole in vacuole o Parasites escpae into cytoplasm quotnakedquot in cell I No vacuole around it so no effect of lysosomes o Manipulate your immune responses 0 Push immune response to THZ which activate a nonprotective antibody response 0 Intracellular 0 Blocks antigen presentation in infected macrophages 0 Inhibits activation of complement cascade in blood 0 Protects trypomastigotes in blood Host Responses 0 CMI 9 cytotoxic T cells 0 Natural killer cells 0 Antibody of no use Diagnosis for Chagas o Enlarged heart 0 Trypomastigotes in blood smear may be difficult 9 recommended method for acute Chagas o Serological tests only for chronic Chagas o ELISA uses flagellar and cytoplasmic proteins of T cruzi epimastigotes to test for host antibody I Use epimastigotes because they re readily available 0 StatPak immunodiagnostic test for host antibodies 0 Chagas RIPA radioimmune precipitation assay fast specific sensitive o Xenodiagnosis Treatment of Chagas 9 Difficult o 2 toxic drugs 0 Both have toxic side effects 0 Don t work for chronic Chagas mainly adults 0 Incomplete cures in acute I Don t get all amastigotes I Incomplete cure rate against trypmostigotes Prevention of Chagas 1 Vector eradication o Pyrethrin sprays roofs and walls of house 0 Limited effectiveness 2 Blood screening 0 2 ELISA tests Leishmania o Obligate intracellular parasites o Heteroxenous o Salivarian o Zoonotic dogs rodents major reservoir hosts 0 Many species 0 Old world and new world species 9 cause same disease Old World Leishmaniasis o L donovani VL o L tropica CL 0 L major MCL CL New World Leishmaniasis o L chagasi VL o L Mexicana CL 0 L braziliensis MCL Vector intermediate host sandfly 0 Old world species phlebotomus 0 New world species lutzomyia 0 Only females bite o Fiercer bite Morhphology of Leishmania 1 Promastigotes develop in sandfly infective stage for humans but will never be found in a human host within r g ofvertebrate host 2 U 0 LD body old name for amastigotes Tissue niche macrophages of host 0 Parasite has to be phagocytosed 0 Only will survive if phagocytosed into macrophages Life cycle picture on moodle 3 Major Clinical Syndromes A Cutaneous Leishmaniasis CL 0 Oriental sore o Chiclero s ulcer ear lesion in New World 0 Middle east India central and South America north America B Mucocutaenous o Espundia uta new world terms 0 Central and south America 0 Middle east C Visceral Cutaneous Leishmaniasis 9 limited to skin and does not invade an internal organs infection remains localized to bite site 0 Old world causes L tropica and L major 0 New world causes L Mexicana and L braziliensis 0 Limited to skin 0 Sandfly bites only occur on exposed ares 0 Can t bite through clothing 0 Progression bite 9 papule 9 cratered ulcer 9 heals with scar 0 Slow process 0 Cratered ulcer has parasites on outside center consists of necrotic tissue 0 mmunity complete with or without treatment Leishmaniasis zoonosis Mucocutaneous Leishmaniasis 0 Starts off as cutaneous 0 New world L brazilienses major species low percentage of cases 0 Old world L major major species very low percentage of cases 0 Metastisis from skin lesion 9 mucocutaneousjunction o Transported by blood hematogenous spread o Lesion erodes into soft tissues skin 9 mucous membranes 9 cartilage o Necrotizing inflammation 0 Necrosis irreversible cellular damage death of cells 0 Disfiguring lesions 0 Nose mouth and throat cavities partially or totally destroyed 0 Treatment is required 0 Heals very slowly o Disfiguring Contrasts and Comparisons 0 Use the same category 0 Don t list facts VL Visceral Leishmaniasis o Kalaazar black fever 0 Leishmania donovani 0 Old world 0 Phlebotomus sp 0 Humans primary reservoir 0 Leishmania chagasi 0 New world 0 Lutzomyia spin LA 0 Humans hutting dogs dogs and foxes Leishman and Donovan 0 Physicians in India during the early 1900 s 1942 human experimentation proved sand fly vector for humans hi mortality rate in human volunteers they were talking about visceral I visceral organs 0 O O O Leishmania donovani Niche macrophages No skin lesion L donovani invades o Spleen 0 Liver 0 Bone marrow o Lymph nodes 0 These are the most seriously affected organs in VL and happen to also happen to be important in immune response Clinical Signssymptoms Slow onset avg 26 mo PI Spleen greatly enlarged splenomegaly o Spleen enlargement makes it bigger than the liver 0 2nd organ in your immune system 0 vascular organa blood I constantly surveys your RBCs to see if they are abnormal old infected the spleen removed them and are destroyed I this is how your RBCs get recycled Liver moderately enlarged 0 Also vascularized organ 0 Normally liver larger in infants and small children but not the spleen o Fever 0 Anemia and thrombocytopenia 0 From bone marrow infection by parasite Usually fatal in untreated 8090 mortality wn 2 yrs 0 Host defenses compromised o Tissues severely damaged 0 Damage to spleen bone marrow lymph nodes affects ability to respond with defense to other organism Can cross placenta 0 Infants born with Kala Azar Most prevalent in children Why 0 Bc children generally play outside more tend to ignore bugs more and wear less clothing Initial signs so nonspecific often not clinically diagnosed Have intermittent high fever but no chills and don t go for medical help until are anemic and spleen is greatly enlarged OO VLand HIV 0 VL causes increasing where HIV endemic 0 HIV infected more susceptible to VL o VL 39 39 HIV quot 39 and this 39 g 39 to AIDS Form of Disease that occurs depends upon 0 Leishmania species involved 0 Geographic location 0 Immune response of host 0 Completely immune to CL 0 Does not provide you with any cross immunity to VL Virulence Factor how parasite is evading host intracellular responses 0 Promatigote Surface coating temporarily blocks lysosomal enzyme action Allows time to transform into amastigote o Amastigote Completely resistant to lysosomal enzymes Parasite promotes activation ofT H2a antibody mediated parasite is intracellular AB not protective Causes severe cellular damage kills infected cells when rupture out Diagnosis of Leishmaniasis by Syndrome Travel history Cutaneous Mucocutaneous Leishmaniasis 0 Biopsy of active lesions Always at outer edge of lesion because the center is necrotic Visceral Leishmaniasis 0 Biopsy of liver spleen or bone marrow for slides To biopsy enlarged liver or spleen since they are so vascularized could be risky due to risk of hemorrhaging 0 Culture of bone marrow aspirate Treatment available Pentavalent antimonial drugs 0 Sodium stibogluconate CL DOC MCL VL 20 days minimum Rx Amphotericin B intractable MCL o Liposomal administration Miltefosine o VL DOC Teratogenic Leshcutan topical oitments CL 0 AKA Paromomycin will speed up the healing 0 Must also use pentavalent antimonial drugs Prevention Get rid of the rodents Avoid sandflies 0 Clothing 0 Repellant Create buffer zones around human habitats Easier said than done in endemic regions Other Flagellates Giardia lamblia and Trichomonas vaginalis 9 pathogens Chilomastis mesnili Retortomonas intestinalis pentatrichomonas hominis Trichomonas tenax 9 commensals Usual mode of transmission fecal contamination of foodwater o T vaginalis obvious exception to this Giardia lamblia 0 Order Dipolomonadida Family Hexamitidae 0 Host humans 0 Distribution is worldwide 0 Host niche small intestine 0 Only parasitic protozoan of small intestion 0 Most common flagellated parasite of GI tract 0 Direct life cycle 0 Morphology trophozoite and cyst infective stage 0 Trophozoite pearshaped 2 nuclei both are transcriptionally active 8 flagella adhesion disc on ventral surface 0 Cyst 4 nuclei 0 Encystment occurs in large intestine 0 Transmission often waterborne o Cyst must be ingested o Reservoirs wild and domestic mammals dogs cats beavers sheep cattle 0 Children most susceptible 9 problem in day cares Soruces of Giardia Cysts 1 Any water supply Chlorination does not kill cysts 2 Unwashed fruits and veggies 3 Objects diapers toys bathroom fixtures 4 Post bathroom usage no hand washing Giardiasis o napparent carrier assymptomatic cyst passers 0 Acute profuse watery diarrhea o Stomach cramps o Bloating and foul smelling flatulence o Rotten egg taste in mouth 0 Chronic prolonged diarrhea episodes 0 Malabsorption 9 weight loss 0 Hypoproteinemia 0 Fat soluble vitamin deficiency Pathology for Giardia o No tissue invasion 0 Feed on mucus secretions doesn t feed on you 0 Physically interferes with nutrient absorption 0 For chronic giardiasis flattened villi malabsportion steatorrhea fatty stool 0 Hosts develop protective immunity 0 IgA antibody involved 0 Can be reinfected Giardiasis Diagnosis 0 Cysts in fecal samples 0 May see only trophs in watery diarrhea o ELISA o Antigen capture tests for antigens distingues current infection 0 1 sample enough 0 Dual kit tests for both Giardia and Cryptosporidium 0 Can also do String test not used often Giardiasis Treatment no alcohol consumption 0 Flagyl metronidazole TID for 5 days 0 Tindamax tinidazole 1 dose 0 Furazolidone for children 0 Lots of fluids Prevention 0 Wash hands 0 Chlorination or idoniation of water 0 Filtration pored with 1 micrometer or less 0 Boil water if not potable 0 Wash fruits and veggies with treated water 0 Don t engage in water sports for 2 weeks after diarrhea stops Trichomonads o Axostyle o Tuft of flagella o Undulating membrane 0 Trophs only 0 Binary fission 0 Direct life cycle 0 All are parasitic Human host Trichomonas vaginalis o Trophs can t survive outside of host 0 Viable up to 24 hours in moist environment 0 STD o Trophs can t survive outside host T vaginalis pathology 0 Trophs attach to epithelial cells 0 Lyse cells and feed on cell contents 9 creates lesions entry point for virus 0 Clinical signs 0 Females tend to be more symptomatic compared to males I Itching burning I Vaginal discharge often odiferous I Can be asymptomatic o Males I Most often asymptomatic Urethritis and discharge can occur 0 Diagnosis 0 Wet mounts of gential secretions o OSOM trichomonas Rapid test I Dipstick ELISA detects parasite antigen I Females only o In vitro culture anaerobic culture medium I Rare transmission to infant during delivery 9 not through placenta 0 Treatment 0 Flagyl all partners must be treated o No immunity Cidal means to kill 0 cidal drugs kill organisms Static means quotto keep checkquot 0 Static drugs stop growth and replication of organisms giving host s immune system time to deal with organisms 0 Not good for an immunocompromised individual Apicomplexans sporeforming protozoa 9 Apicomplexans I which are intestinal and tissue parasites All have an apical complex spore stage Alternate between asexual and sexual reproduction Have an apicoplast 0 Found in most 0 Organelle is considered relic of a chloroplast 0 Contains genes essential for survival of parasite Apical complex is found in sporozoite and merozoite stages 9 only used to enter into host cell 0 Polar ring conoid rhoptry micronemes subpellicular tubules o Differentiate and disappear after penetration into host cell 0 Process 0 Adhesion proteins released by apical complex 0 Parasite pulls host membrane over like quotputting on a sock o Avoids getting a lysosomal response Terminology o Schizogony multiple fission that beings with sporozoites and produces merozoites o Merogony means same thing multiple fission to produce many daughter cells 0 Gametogony merozoite differentiating into gametocytes o Syngamy fusion of macrogamete and microgamete forms zygote o Oocyst virally resistant form of zygote that has sporozoites o Sporogony Family Eimeriida o No Eimeria spp infect humans 0 sospora belli pathogen 9 direct life cycle 0 Cyclospora cayetanensis pathogen 9 direct life cycle Family Cryptosporidiidae o Cryptosporidium parvum pathogen 9 direct life cycle Family Sa rcocystidae o Toxoplasma gondii pathogen 9 indirect life cycle 0 Sa rcocystis spp Schizogony 0 Multiple fission o Nucleus divides multiple times 0 Undergoes one cytokinesis 0 Results in multiple daughter cells from 1 parent 0 Called o Merogony merozoites o Sporogony sporozoites o Gametogony gametes 3 Phases in Apicomplexan Life Cycle 0 Merogony within host 0 Gametogony within host 0 Sporogony usually outside host 0 Sporozoites infective stage 0 Contained within sporocyst 0 New host must ingest sporulated oocyst Eimeria oocyst 4 sporocysts with 2 sporozoites each sospora oocyst 2 sporocysts with 4 sporozoites each Eimeria tenella affects chickens o Morbidity number of people that get sick and mortality those who get sick and die 9 both are high 0 Niche ceca epithelial cells of lining o Ingestion of sporulated oocysts in feed or water 0 Merogony occurs in epithelial cells of cecum o Gametogony in same place 0 Sporogony outside host 0 Host defenses o Shed cells 0 Fecal express 0 macrophages Unsporulated oocysts aren t infective Isospora belli 0 Only isospora species to infect man 0 Distribution tropical not USA 0 Profuse watery diarrhea abdominal cramping fever 0 Immunocompromised individuals 0 Infants and young children 0 Least common of intestinal coccidian that infect humans 0 Niche small intestine 0 Diagnosis oocysts in fecal sample 0 Treatment TMPSMX Bactrim Cyclospora cayetanensis fairly new 0 Worldwide 9 considered emerging pathogen o Niche jejunum of small intestine o Explosive watery diarrhea o Cramping abdominal pain 0 Vomiting o Persists several weeks 0 Selflimiting 0 Sources 0 Contaminated food 0 Contaminated water 0 Oocyst 2 sporocysts with 2 sporozoites each 0 Very refractile not easily visualized in unstained fecal sample 0 Acidfast stain 9 see reddish oocyst quite large 0 Diagnosis acid fast stain of fecal smear look at size bar very large compared to others 0 Treatment same for isospora Cryptosporiididae Family 0 Worldwide o Zoonosis only host specificity is vertebrates 9 mammals birds reptiles fish 0 Not host speci c 0 2 species infect humans 0 Cryptosporidium parvum o Immunocompromised infants and elderly at risk 0 No apicoplast 9 apicoplast genes still present but they have been moved to the nucleus 0 Direct life cycle 0 Sporogony occurs inside 9 internal sporulation I u n I u I 0 Don t go InsIde cell created I Does have host cell membrane around it but can t be recognized by lysosomes within cell 0 2 types of oocysts with no sporocysts 9 only 4 sporozoites I Thickwalled go out in feces very resistant to environment infective stage 0 v Survive weeks to months in moist envirobnments 39239 Resistant to chlorination I Thinwalled attach to epithelial cells rupture in GI tract 9 autoinfection never left body 39239 Reinfection within host 0 Merogony and gametogony within fused microvilli of epithelial cells 9 entire GI tract host niche Clinical Cryptosporoidosis o Profuse watery diarrhea abdominal pain nausea and vomiting 0 ln immunocompetent host 0 12 weeks duration 0 Selflimiting o In immunocompromised host 0 Becomes chronic and persistent 0 Can be fatal includes infants and elderly 0 Pathology 0 Fluid and electrolyte loss 0 Asymptomatic carriers 0 No clinical signs 0 Shed infective oocysts 9 can infect others 0 Route of transmission 1 Waterborne lakes swimming pools water parks contaminated municipal water supply 2 Foodborne filth flies poor hygiene of infected handlers 3 Day care centers 4 Lab techs oocysts in fecal samples infective Diarrhea lasting longer than a week 9 Giradia lamblia or Cryptosporidium parvum Cryptosporoidosis Diagnosis 0 Acid fast stain of fecal sample much smaller size of oocyst o ELISA kits 0 Dual kit for both Cryptosporidium and Giardia o lntestinal biopsy 0 After negative results from less invasive diagnostic techniques Crypto Treatment 0 Nitazoxanide Alinia not effective for immunocompromised HIV 9 Static drug 0 Plus fluid and electrolyte replacement 0 Immunity does develop 0 Can get reinfected o Requires larger infective does 0 Symptoms milder 0 Can be fatal in immunocompromised Crypto Prevention 0 Sanitation and hygiene o Prevent fecal contamination of water supply 0 Municipal water courses lakes rivers 0 Need filters 1 micrometer or less because oocysts are so small Fa m ily Sa rcocystidae 0 Include Toxoplasma gondii and Sarcocystis spp o Heteroxenous o Asexual reproduction in intermediate vertebrate hosts 0 Sexual reproduction in definitive vertebrate hosts 0 Life cycle stages 9 both intestinal and extraintestinal tissue stages 0 Tachyzoites formed by multiple divisions in extraintestinal cells somewhat analogous to merozoites in gut o Bradyzoites dormant tachyzoites transform into this stage in tissue cysts in extraintestinal sites 0 Zoitocysts tissue cyst aka bradycyst Toxoplasma of pseudocyst Sarcocystis Toxoplasma gondii 0 Worldwide o Obligate intracellular parasite 0 Only 1 genes and species 0 Heteroxenous 0 Intermediate hosts requires warm blooded animals any nucleated cells includes mouse humans other mammals and birds 0 Definitve host cat only only ones that will produce oocys1s I Usually asymptomatic I Sporogony occurs outside in environment 0 Life cycle 0 Intestinal stages ingested oocysts or bradycysts both go to merozoites and then gametogony o Oocysts can get into blood and pass through placenta to fetus Transmission to Human Host 1 Ingestion of tissue cysts bradyzoite eating rawundercooked meat 2 Ingestion of sporulated oocyst sporozoite 3 Transplacental tachyzoite 4 Blood transfusion if not screened 9 tachyzoite 5 Organ transplant Tachyzoites can t survive in stomach if digested but bradyzoites can Toxoplasma gondii evades host cell defenses 9 intracellular defenses o Prevents fusion of lysosome with parasite vacuole I Prevents fusion of lysosome with parasite vacuole I Accumulation of host cell mitochondria around vacuole Toxoplasmosis in Man 0 Clinicalsyndromes 0 Acquired o Congenital o Recrudescent o individualsatrisk o mmunocompromised I Organ transplant recipient I HIV I mmunosuppressivetreatment o Fetus Acquired Toxoplasmosis o mmunocompetent hosts 0 Benign with few to no symptoms 0 Asymptomatic or very mild flulike 0 Possible swollen lymph nodes ex cervical nodes 0 Have tachyzoitesparasitemiatissue damage 0 Bradycysts with bradyzoites dormant from when immunity develops Chronic Infection 0 mmunocompetent hosts 0 Immunity develops 9 organism transforms to bradyzoite o Bradycyst formation 0 Tissue predilection brain muscle skeletal and heart eye 0 Organisms dormant o No inflammatory response to bradycycsts o Immunity complete Congenital Toxoplasmosis mom is not at risk can t say that fetus will get parasite if mom is infected o Tachyzoites can cross placenta 0 Mom must have acute toxo with parasitemia she becomes pregnant 0 Infection in fetus o Varied clinical picture 0 Gestation period at time of infection 0 Infective does size 0 1st trimester infection rates lowest but parasite damage greatest 0 3rd trimester infection rates highest but parasite damage least 0 Born symptomatic classic triad of signs 0 Hydrocephaly o ntracranial calcification of cysts o Chorioretinitis 0 Born asymptomatic but problems later 0 Seizures 0 Mental retardation 0 Visual problems 0 Born asymptomatic 9 no effects at all Possible Severe Consequences to Fetus won t necessarily happen 0 Mental retardation o Blindness o Seizure 0 Hearing loss 0 Death stillbirths abortions Recrudescent Toxo o mmunocompromised loss of immunity bradyzoites 9 tachyzoites 0 Brain 9 encephailits cerebral toxo 0 Heart 9 mycocarditis 0 Eye 9 chorioretinitis ocular toxo o In GI tract liver lung skin possible Toxo Diagnosis 0 Antibody detection IgG and lgM 0 PCR detection of o CSF ocular fluid 0 Prenatal and neonate amniotic fluid IgM can t cross the placental barrier to so detection of IgM means it came from fetus IgM and IgG 9 wait 2 weeks for immune response 0 lgG also indicates individual just got infected o If not positive then false positive and no infection IgM typically produced only in first contact Ability of T gondii to evade host cell defesnses o Intracellulardefenses RX 0 Fetal toxoplasmosis o Spiramycin DOC 0 Given to mom to cross placenta to the fetus o Antibiotic o mmunocompromised o Pyramethamine sulfadiazine o Folic acid antagonists 0 Cannot give during pregnancy due to the risk of developing spina bifida and other birth defects 0 Congenitally infected neonate after birth 0 Pyramethaminesulfadiazine folinic acid 0 A preventable disease 0 Cool all meat Freezing salting smoking pickling with not reliably kill bradyzoites Wash raw fruits and veggies Pregnant women wear gloves when gardening 0 Don t clean cat litter box o If you have to make sure you do it everyday because the chances are you are not going to have any sporulated oocysts o If you have cat keep it indoors 0 Wash hands immediately after stroking cat that is free roaming o Oocyst can cling to fur Sarcocystis spp o Herbivorous intermediate host 0 Carnivorous definitive host 0 Not pathogenic in humans 0 Humans definitive host Sarcocystis hominis o Infective stage for intermediate host 0 Sporozoites in sporocyst definitive host don t shed oocyts 0 Internal sporulation and ruture of thin walled oocyst in gut o Sporocysts with sprozoites out in feces o Infective stage for definitive host 0 Bradyzoites in tissue cyst You can see sa rcocysts with the naked eye Apicomplexans Chapter 9 Organisms that cause malaria and malaria like diseases Genus Plasmodium Species falciparum vivax ovale malariae Genus Babesia Species bigemina microti divergens canis Plasmodium spp 0 One stage must be blood of vertebrate host Heteroxenous 0 Cannot use the term definitve host or intermediate host 0 Merogony and 151 part of gametogonyIJertebrate host 0 2quotd part of gametogony and sporogonyllnvertebrate hostlyector mosquito infective stage for vertebrate hostlporozoite infective stage for vector ametocytes 1st pa rt from the blood of vertebrate host The liver is always the first place where malaria parasite goes o It is the only place with the receptor Ookinete motile zygote in vector produced in sexual reproductionHemozoin insoluble pigment in RBC s is end product of parasite digestion of hemoglobin Circumsporozoite protein protein on surface of Plasmodium sporozoite that attaches to receptor on hepatocyte This allows sporozoite to enter the liver cell Cryptozoite schizont in liver Hypnozoite sporozoite in liver that goes dormant instead of transforming into trophozoite and undergoing schizogony can remain viable for years source of organisms in relapsing malaria P vivax amp P ovale Schuffner s dots appear as stippling in RBC cytoplasm actually invaginations of RBC plasma membrane Ring Stage young trophozoite in blood cell cytoplasm is visible as thin rim around central vacuole in parasite with nucleus of parasite as a reddish purple dot at the edge Tertian malaria periodicity in schizogony results in RBC rupture every 48 hours Quartan malaria periodicity results in release every 72 hrs Relapsing malaria reinfection of RBC s and reappearance of clinical signs from activation of hypnozoites in liver 0 Plasmodium vivax and Plasmodium ovale only Recrudescing malaria flare up of active disease from very low level of infection being maintained in RBC s No exoerythrocytic hepatic stages involved 0 Plasmodium falciparum and Plasmodium malariae only Induced malaria mechanical transmission of malaria organisms from blood of infected individual via syringes blood transfusion during delivery to neonate No exoerythrocytic hepatic stages involved Congenital malaria transmission across placental barrier to fetus Very rare but can occur No exoerythrocytic hepatic stages involved 0 Periodicity to recur at regular intervals for malaria the recurring episodes of fever amp chills Malaria 0 100000 year old parasite o Hippocrates and Galen 500 BC 0 4 Plasmodium species that infect man 0 are not phylogenetically related 0 Vector Anopheles spp mosquitos 60 species 0 1 killer of children and pregnant women 0 tropical and subtropical regions 0 falciparum 0 this is a genetic term make sure on the test you are specific 0 Major disease in tropical and subtropical regions of world 0 Endemic disease eradicated form most temperate regions but can occur anywhere a vector is found 0 27 million death per year Transmission of malaria o bite of infected mosquito the major way parasite transmitted 0 Blood transfusions from infected donor 0 A problem only in areas where donors are not screened 0 Mechanical dirty syringes o Neonate infected during delivery Exoerythrocytic cycle 0 Schizogony in liver o P falciparum has the most merozoitessporozoites 40000 Type of Malaria by each species 0 P falciparum 9 malignant tertian malaria o P vivaz 9 benign tertian malaria o P malaria 9 quartan malaria o P ovale 9 mild tertian Paroxysm sudden onset of recurrent signs of symptoms 0 Ex periodic spasms of fever and chills in malaria 0 Based on what the parasite is doing within RBCs Rigor 0 Cold stage paroxysmal chills with high fever and shivering 0 Hot stage sense of being very hot with severe headache dizziness nausea etc o Fever has subsided o Profuse swelling Classic Clinical Signs 0 Cyclic fever 104106 o Chills o Headache o Myalgia ache all over flu like 0 Malaise and lethargy o Anemia parasite killing RBCs o ntravascularhemolysis 0 Bone marrow suppression o Enlarged liver and spleen o Nausea vomiting diarrhea small children 0 Jaundice Two Major Factors for Pathogenesis 1 RBC destruction 2 Host inflammatory responses Malignant Tertian Malaria 0 Most prevalent type over 50 0 Most pathogenic 0 Highest mortality rate I Especially in children pregnant women elderly 0 High fatality rate in all if untreated 0 Can recrudesce but not relapse Why is P falciparum the most pathogenic a 40000 merozoites per sporozoite b nfects all ages of RBCs 25 RBCs infected is fatal 0 Greatest parasitemia levels 0 Greatest destruction of RBCs 9 hemolysis of both infected and uninfected RBCs c Deep vascular schizogony o RBCs sequester in capillaries of major organs d Drug resistance Deep vascular schizogony o This is why only iriy ring stages and gametocytes seen in peripheral blood 0 Infected RBCs sequester in blood vessels of major organs 0 Capillary beds congested with infected RBCs o Parasite induces protein quotknobquot on RBC membrane 0 Helps bind parasite to endothelial cells of capillary 0 Pregnant woman sequester in placental vessels Why sequestration o Parasite defense 9 prevents premature destruction of infected RBCs by spleen o Allows parasite to continue life cycle development Tertian malaria merogony is every 48 hours Only forms seen in peripheral blood 0 Early rings 0 May be multiple rings in 1 RBC 0 Bananashaped gametocytes which are infective stage for mosquito o Appear about 10 DPI o Viable for 4 days Organs become black from hemozoin as a result of RBCs being destroyed Falciparum Malaria Malignant Tertian 0 Severe anemia worst than in all other malarias RBC infected and uninfected destroyed O 0 Loss of iron because it s bound to hemozoin waste product 0 Decreased production of RBCs I Bone marrow suppression I No RBCs being produced I Can t recycle iron in hemozoin I Decrease in WBC production 0 Host inflammatory response Possible consequences of falciparum 0 Severe malaria 9 means severe parasitic infection 0 Cerebral malaria check with Nicole 0 Always fatal if untreated within 2472 hours 0 Doesn t cause permanent damage 0 Coma symptoms I unconscious with no response to pain I hyperthermia up to 108 39 peripheral r 39 very high I convulsionsseizures Coma pathogensis 2 hypothesis A Mechanical 9 hypoxia B Biochemical 9 nitric oxide effect 0 0 Renal failure Results of Massive Hemolysis of RBCs 1 Severe anemia and leucocytopenia Very low RBC and WBC numbers Caused by hemolysis and bone marrow suppression O O 2 Hemoglobinuria 3 Jaundice 0 Liver can t handle overload of hemoglobin breakdown products 0 Liver can t metabolize all the bilirubin 0 Excess bilirubin is deposited into tissues Kidney o Filters soluble substances 9 only things dissolved in plasma 0 Can t filter insoluble or particulate substances Hemoglobinuria spillover of hemoglobin into urine result of massive hemolysis Hematuria intact RBCs in urine only from bleeding lesion in urinary tract 9 not filtration of blood from kidneys Hemozoin insoluble black pigment solid waste from parasite digestion of hemoglobin Never found in urine Renal Effect llBlack Water Fever 0 Hemoglobinuria o Damage to kidney at glomerulus 9 tubular necrosis 0 Leads to renal failure 9 death 0 Not common sequel to faliparum malaria P falciparum in Pregnant Women 0 Signs severe anemia hypoglycemia very high fevers toxemia o 400x greater risk of fatality 0 Pregnancy dampens maternal immunity 0 Not immunosuppressed o Fetus often dies Causes of Fetal Death 0 Indirect effect 9 all caused by mom s complications 0 Anoxia 0 From mom s severe anemia 0 Lack of oxygen for fetus o Hyperthermia 0 From mom s high fever 0 Makes uterus like an oven 0 Temperature of fetus also climbs o If fetus survives 0 Low birth weight 0 Often succumbs to other childhood illnesses Reminders 0 Children 0 Pregnant women 0 Immunocompromised and elderly Falciparum is most prevalent and most pathogenic of Plasmodium spp infecting man Benign Tertian Malaria Plasmodium vivax o Temperate and tropical zones not common in South Africa 0 All stages of parasite seen in peripheral blood 0 RBCs enlarged and stippled with Schuffner s dots o Infects only reticulocytes very young 0 No multiple infections of 1 RBC 0 Relapsing fever 0 Hypmozoites in liver 9 reappeatance of malaria 58 years 0 Can follow after treatment and recovery from malaria Comparing Periodicity o P vivax gives 48 hour period break 0 P malaria gives 72 hour break 0 P falciparum hardly gives a break Quartan Malaria Plasmodium malariae o Tends to be a milder infection 0 Much lower number of merozoitessporozoite o Infects older RBCs o Longer between cycles of RBC hemolysis 0 Can have clinical signs before parasitemia detectable 0 Can recrudesce o Considred infected for life 0 Can persist clinically undetectable fro 5060 years Blood Smear o No multiple infectionscell o No RBC enlargement 0 Band shaped trophozoite across RBC Plasmodium ovale 0 Clinical disease similar to P vivax Innate Resistance to Malaria Genetic Factors 0 Duffy blood group recessive 9 specific to P vivax only 0 Sickle cell trait heterozygous carrier 0 Carriers defective version of hemoglobin o GGPDH deficient individuals 0 Beta thalassemia Immunity 0 Acquired antibody mediated 0 Infants antibodies in breast milk 0 Weaned children are the most susceptible o Premunition low level of parasitemia blocks new infection 0 Complete sterile cure 9 susceptible again Why does CMI not work 0 RBCs don t have HMC1 molecules and can t be sent to cytotoxic T cells Diagnosis of Malaria o Microscopy stained peripheral blood smears o ELISAL antigen capture optimal 0 Measures parasite enzyme positive active infection 0 IFA antibody detection in patient serum o PCR Any prolonged fever of unknown origin regardless of travel history 9 malaria should be considered Treatment of Malaria o Quinine no resistant yet 0 Not used much because of serious side effects 0 Reserved for severe cases andor resistant malaria specied O Selectively cidal I Kills meroizites schizonts I No effect on sporozoites liver stages or gametocytes 0 Major side effects I Ringing in ears tinnitus 9 hearing loss I Increase in RBC hemolysis I Increase insulin output by pancreas 9 hypoglycemic shock I Fetotoxic causes abortions I Cardiotoxicity 9 can cause serious cardiac arrythmias o DOC 9 cerebral malaria 0 Severe P falciparum infection 0 Rapidly absorbed and distributed in body 0 Chloroquine o Cidal kills parasites 0 Synthetic quinine related drug but without its side effects 0 P falciparum resistant worldwide 0 Mefloquine o Atovaquone proguanil Malarone o Primaquine o ills hypnozoites meaning the liver stages no effect on P falciparum or P malaria o No effect on RBCs o Artemisinins plant derivatives 0 Artesunate o For cerebral malaria and can t take quininequinidine Antibiotics in combo with quinine in chloroquin restant falciparum cases 0 Ex clindamycin doaxcycline tetracycline o Attacks mitochondial DNA 0 Apicomplexans have apicomplast with its own DNA Recommendations for Malaria Treatment US 0 Assume falciparum malaria until ID d 0 Immediate treatment with o Atovaquoneproguanil o mefloquine o If severe quinine with doxycycline or clindamycin o If not falciparum can use chloroquin CDC Travel Recommendations 1 Prophylaxis before during and after trip 9 don t skip doses 2 Sleep under netting 3 Clothing that covers 4 Repellants DEET Prevention in Endemic Regions 0 Vector reduction 0 Minimize contact with mosquitos o Chemotherapy Babesia spp 0 Biological vector tick o Zoonosis 0 Disease ranges from mild rever to life threatnening 0 Human medicine 9 Emerging infections 0 Veternivary medicine 9 been around for a while Babesia bigemina 0 Host cattle primarily humans 0 Vector Boophilus annulatus B microti 0 Host humans rodents 0 Vector Ixodes scapularis deer tick B duncani 0 Host humans 0 Vector unknown B divergens 0 Host cattle humans Europe 0 Vector Ixodes ricinus B canis 0 Host dogs 0 Vector Rhipicephalus sanguineous brown dog tick and Dermacentor variabilis American dog tick General Life Cycle Vertebrate Host 0 Infective stage sporozoite o Invade RBCs no liver cycle 0 Feeds on hemoglobin but no hemozoin o Binary fission 9 merozoites o Intrvasuclar hemolysis o Gametogony gametocytes in vertebrate host 9 ray bodies gametes in tick host Tick Host 0 Sexual reproduction 0 Transformation of gametocytes into ray bodies 0 Fusion of ray bodies 9 motile kinete o Sporogony o Sporozoites go out in saliva Tick species as vector will determine mammalian host some organisms are more specific than others 1 host tick entire life cycle on 1 host transovarial transmission 2 host tick larva and nymph on 1st host and adult on 2nd 3 host tick larva on 15 nymph on 2nd and adult on 3rd Ticks attracted to CO2 emissions wait for host to come by Babesiosis in Man Nantucket Fever 0 Babesia microti o Infects rodents humans etc Clinical presentation headaches fever malaise about 2 weeks Mild and selflimiting in immunocompetent individuals Population at risk 0 mmunocompromised o Splenectomized 0 Can be life threatening with hemolytic crisis and severe anemia Spleen s nonimmune role in defense 0 Detects all abnormal RBCs filtering through sinuses in organ and infected RBCS phagocytized by resident macrophages B bigemina o Babesiosis in cattle 0 quotTexas tick fever or quotred water fever 0 Anemia o Hemoglobinuria 0 High mortality rate in adult cattle but young cattle have premunition and are protected 0 Vector Boophilus annulatus o Eliminated in USA but it is not eradicated in Mexico so you must keep high surveillance 0 Incomplete metamorphosis no pupa stage 0 Egg9larva9nymphs9adult o Transovarial transmission I When the tick is infected the parasites will infect the eggs When the eggs hatch they are already infected I 1 host ticks 2 host ticks I 3 host ticks Babesiosis Treatment antimalarial drug with antibiotic o Clindamycin quinine o Azithromycin atovaquone Helminths 2 major groups platyhelminthesflatworms and nematodesround worms Acoelomic no body cavity Bilaterally symmetrical Obligate parasites can t survive outside host Digestibe system primitive tract ending in blind sac o In trematodes 0 Absent in cestodes Have nervous muscular excretory system Reproduction o Monoceious cestodes and most trematodes o Diecious schistosomes only Digenetic trematodes flukes 0 Development requires 2 hosts 0 15 snail o 2quotd vertebrate some may have 23 intermediate hosts General Trematode Life Cycle egg 9 miracidium 9 sporocyst 9 redia 9 cercaria 9 meetacercaria 9 adult Asexual is always in the snail definitive hosts human has sexual reproduction Egg miracidium cercaria and adult in all species Egg 0 Opercuclum allows miracidium to leave 0 Hatching water is essential o Freezing drying are fatal will kill miracidium Miracidium o Ciliated and freeswimming 0 Needs snail host quickly 0 Mucous trail of snail attracts it 0 Some species require snail to eat it Sporocyst o Metamorphosis of miracidium in snail o No mouth or digestive system 0 Germinal sac asexual reproduction Redia o More advanced germinal sac 9 has oral sucker o Mouth pharynx short gut 0 Feed on host tissues sporocysts other redia 0 Produce more embryos 9 daughter redia Cercaria 0 Juvenile stage 0 Mouth and digestive e system 0 Penetration glands at anterior to O 0 Can be infective stage for vertebrate hosts Metacercaria o Encysted form of metacerca ria 0 Intermediate host if 2nd int host 0 On aquatic vegetation if no 2nd int host 0 Must be ingested by vertebrate host Value of metacercarial stage 0 Longervhb hy o Mans of transmission to definitive host How trematodes infect definitive host 0 Direct penetration 9 cercaria o Ingestion on metacercaria either in intermediate host or on plants 3 reproductive strategies all are sexual reproduction and require fusion of sperm and egg 1 Selffertilize ex Fascioloa hepatica 2 Cross fertilize Paragonimus westermani 3 Separate sexes Schistosomes Intermediate hosts snail Definitive hosts humans other mammals birds turtles fish Mature in vascular system blood of host Schistosomiasis 0 Distribution Africa Asia South America Caribbean 0 Chronkdeb ha ng S heomatboium japonicum far east mansoni Caribbean South America 9 only one in new world Dioecious separate sexes o PMrupinhumanho o Remain paired for life in copula o Dimorphic o Males larger shorter I Has gynecophoral groove where female stays 0 Females smaller and longer Hostnkhe o Schistosoma haemitobium can never cause liver problems 0 Unrivary bladder veins 9 causes urinary tract disease 0 No known animal reservoirs o Schistosoma japonicum 0 Superior mesenteric veins small intestine 9 cause intestine and liver disease 0 Zoonosis 0 Major reservoirs cattle water buffalo o Schistosoma mansoni o Inferior mesenteric veins large intestine 9 causes intestine and liver disease 0 No animal reservoirs Schistosome eggs 0 S haematobium ovoid with terminal spine 0 S mansoni ovoid with lateral spine on the side 0 S japonicum round with rudimentary spine small bump 9 not always seen Schistosome Life Cycle Egg requires water 9 miricidiumeach will give rise to only one sex9 sporocyst 2 generations9 cercaria 9 adult 0 Intermediate host snail o Definitive host humans by cercaria o 3 month cycle from egg to egg Snail hosts no snails capable of vectors for human schistosome spp o S mansoni Biomphalaria spp o S japnicum Oncomelania spp o S haematobium Bulinus spp Schistosome Cercaria o Attracted to skin secretions amino acids and fatty acids 0 Process 0 Attach to skin 0 Release chemicals to signal others 0 Creep to hair follicle o Penetrate skin loses tail sheds outer coat insde o 30 min to get inside host 0 Sheds outer coat when it enters host Why 0 Cercaria has to first survive in hypertonic environment Schistosomule little schistosome o Capillaries 0 Heart 9 lung 9 heart 0 Liver 9 venous plexus 0 Stay in liver for about a month 0 Mature and mate pair up Host vs Parasite o Evades host defenses by camouflage 1 Coats its outer surface with host plasma proteins 2 Produces surface molecule on their outer membranes that mimics part of vertebrate host MHC 1 o Schistosomule 9 adult 0 Hidden from immune system as host self 0 What causes problems I Eggs cause direct tissue trauma trigger host inflammatory and immune response Eggs must travel through host tissue to organ lumen o S mansoni and S japnicum intestine 9 feces o S haematobium bladder 9 urine Eggs Secrete SEAs soluble egg antigens o Hydrolytic enzymes 0 Trigger large host inflammatory response 0 Stimulate granuloma formation macrophages eosinophils lymphocytes around eggs 0 Stimulate production of TNFalpha by macrophages 0 Very antigenic o Trigger host immune responses About 66 eggs don t make it 0 Get trapped in walls of organs 3 Phases of Schistosomiasis 1 Migratory asymptomatic o Penetration 9 host niche site 0 Repeated infections 9 transient cercarial dermatitis at penetration site I sensisitization 9 34 days O In lungs must cross from venous to arterial side possible cough and low fever when in lungs if heavy infection 2 Acute Katayama Fever 0 0 Heavy initial infections mansoni japonicum Signs occur with onset of egg production Eggs may not be detectible in feces yet Flulike fever and chills myalgia enlarged lymph nodes Inflammatory and immune response I TNFalpha by macrophages serves as quotvitaminquot for patasite enhances egg production 3 Chronic repeated exposure to heavy infections 9 takes years 0 O O O Intestinal and liver problems mansoni and japonicum Urinary tract problems haematobium Result of trapped eggs I Chronic granulomas around eggs 9 fibrosis and calcification I Remain active so still causing immune response Intestinal problems abdominal pain chronic diarrhea I Possible bloody diarrhea granulomas in intestinal wall 9 ulcerating I Can cause anemia and irion deficiency especially in children I Gut wall fibrosis 0 00 Erosions ulcers fibrosis around tissue masses called pseudotubercles o 00 Eggs within granulomas are biable SEAs still released 0 00 Buildup of fibrosis 9 difficult for eggs to pass thru now 0 00 Can form polyps extending into gut lumen 9 gut obstruction Intestinal Problems 9 Liver Problems Eggs swept to lover and get trapped in small veins which forms granulomas around eggs in veins Periportal fibrosis pipestem fibrosis in and around vein occlusion of small veins that leads to resistance to blood flow Portal hypertension interfering with blood flow in liver Shunting to spleen and same situation occurs there Liver problems 0 Liver fibrosis occurs within and around blood vessels 0 Enlarged liver and spleen 0 Portal hypertension S haematobium o Bladder wall fibrosis and calcification 0 Loss of elasticity decreased bladder capacity 0 Can cause retrograde UT problems 0 Possible cancer development Very Severe Chronic Schistosmiasis 0 Small number infected with S mansoni or S japonicum 0 Liver fibrosis extremely sever o Enlarged liver 0 Severe portal hypertension increased resistance to blood flow in liver vessels 0 Greatly enlarged spleen 0 End result chronic passive congestion of liver 0 Ascites fluid accumulation in abdominal cavity Hepatic portal vein does not become blocked by eggs 0 Eggs are microscopic and plug up small vessels such as capillaries Resistant to Blood Flow in Liver 0 Passive congestion of liver 0 Formation of ascites and major shunting of eggs to spleen 0 Starting problems in spleen 0 End result ascites hepatomegaly andsplenomegaly S mansoni 9 pipe stem fibrosis in liver around blood vessels Impaired Blood Flow and Portal Hypertension 0 Liver produces collateral circulation o Allows eggs to bypass liver and get to lungs 0 Loss of functioning lung tissue 0 Pulmonary hypertension 0 Heart failure can result Egg production 0 S japonicum is most pathogenic and its eggs are more likely to go to ectopic abnormal locations brain lesions 0 May have few to none in feces with a chronic infection Squamous cell carcinoma of bladder 9 caused by S haematobium Complications by S Haematobium 0 Pain on urination o Hematuria whole blood cells in urine develops gradually 0 Eggs trapped in bladder wall 9 calcification and fibrosis of bladder wall 9 loss of bladder elasticity 9 increased frequency of urination o Polyp formation granuloma forms around eggs and trapped them 0 Common sequelae bladder cancer squamous cell carcinoma of bladder Hydronephros and hydroureter backup of urine from bladder causes extreme pressure to cause renal failure Diagnosis of Schistomiasis 0 Find eggs urine haematobium feces japonicum and mansoni o Buildup of chronic fibrous tissue in gut and bladder prevents eggs from passing out so not found in feces or urine 0 Rectal or bladder biopsy to find trapped eggs o ELISA 0 Not good for japonicum 0 Specificity varies according to species 0 Sensitivity poor 0 Best time to collect urine sample is around noon 9 when egg excretion is maximal Transmission Requirements 2 o Fecalurine contamination of water sources 0 Snail vector present 0 Risk factors Traditions and customs O 0 Human wastes for fertilizer o Streams as human waste disposal sites 0 Wading bathing playing in contaminated water S mansoni is the only one found in the new world South America Treatment 0 Praziquantel DOC o Effacicius 1 dose kills all adults 0 Low number of side effects 0 Low cost 0 Mechanism ofaction dual effect 1 Disrupts parasite s tegument quotunmasksquot worm 9 causes them to lose protein 2 Disrupts flow of calcium ions in nervous system of worm killing it Immunity Concomitant 0 Type of protective immunity 0 Takes years to develop 0 No effect on adults 0 Stops cercaria prevents new infections and an increasing worm burden Removal of adults sterile cure host susceptible to reinfection PreventionControl 0 Education 0 Cure infected individuals 0 Vector control difficult and some chemicals not ecofriendly o Vaccines not yet achieved Cercarial dermatitis o Swimmers itchSwamp itchnutria itch 0 Infection w cercaria of other schistosomes o Maculopapular rash 0 No uid 0 You can be infected by schistosomes in USA It isn t made for humans so you will kill it but it still is annoying humans cannot get schistosomiasis 0 Infection with cercaria killed by immune response Trematodes o Hermaphroditic 0 Most selffertilize 0 Intermediate host aquatic snail Liver flukes o Fasciola hepatica o Fasciolopsis buski exception intestinal fluke o Fasciola gigantic o Fascioloides magna Fasciola hepatica quotliver rotquot 0 Sheep liver fluke 0 Worldwide 9 common in southwest USA 0 Intermediate host Lymnea spp other related snails worldwide 0 Definitive hosts sheep cattle humans 0 Host niche liver 9 bile ducts to be more specific 0 Have very characteristic morphology prominent anterior con with quotshouldersquot also large 35mm 0 Life cycle stages egg 9 miracidium 9 sporocyst 9 redia 9 cercaria 9 metacercaria 9 adult 0 Metacercaria infective stage for definitive host 0 Life cycle life span 1112 years 0 Metacercaria excyst in SI 0 Penetrates gut wall 0 Across peritoneal cavity to liver 0 Matures 0 Adults burrow through liver during life span 0 Feed on liver cells and bile duct epithelium o Create necrotic tracks in liver 0 Eggs out via bile duct to GI tract and out in feces 0 Human infection requires 0 Fecal contamination of water 0 Ingestion of metacercaria I Eating aquatic vegetation watercress water caltrop water chestnuts I Drinking water with metacercaria 9 possible but not probable 0 Adult flukes o Secrete proline I Parasite version causes bile duct epithelium to proliferate hyperplasia and cells to enlarge hypertrophy I Cultivates some of their food gardening in bile duct 0 Clinical disease 9 fascioliasis 0 Liver damage caused by migration and feeding of flukes I Abdominal pain over liver upper right quadrant I Can cause liver abscesses 0 Heavy infections I Bile duct obstruction 9 liver damage 39239 Pipestem fibrosis around bile ducts I Gall bladder damage 0 No portal hypertension F hepatica 0 Economic loss in herbivores o Condemned livers o Decreased production of milkmeat 0 Poor growth of young infected animals 0 Humans o Rarely infected remember that this is a worldwide disease so the number of human infections compared to the large distribution is relatively small 0 But if infected RX to prevent permanent liver damage Halzoun 9 common in Mideast o Pharyngitis with pharyngeal and laryngeal edema pain 0 After eating delicacy quotraw sheep liver 0 F hepatica thought to be cause 0 Adults in sheep liver attach to back of throat 0 Actual cause tongue worm Linguatula serrata Diagnosis 0 Eggs in fecal sample 0 ELISA tests for host antibodies 0 Crossreactivity with other parasites Treatment 0 Trichabendazole cidal drug 0 Interferes with microtubule formation o Stops all cellular functions requiring microtubules 0 Only fluke that Praziquantel is not the Doc 0 15 requires 100x usual dose 0 2 that increased doses greatly increases side effects 0 3 increased does not kill all parasites Pseudofascioliasis o asymptomatic 0 False positive for infection with Fasciola hepatica 0 Result of eating infected beef or sheep liver with eggs 0 Eggs pass on through GI tract 0 Eggs out in feces o Recheck after liver free diet for 2 weeks Why can you not get infected from meat with eggs 0 Not next host for development 0 Requires snail Prevention 0 Reservoirs keep pastures infected o Snail control is difficult 0 Ability of snail host to aestivate in dry conditions 0 Prevent fecal contamination of water sources 0 difficult 0 Best way don t eat unwashed fresh veggies Fasciola gigantic 0 Similar shape to hepatica but much larger 0 Same life cucle Fascioloides magna Liver fluke 0 Similar to F hepatica life cycle and size 0 Except in liver tissue not bile ducts 0 Doesn t infect humans 0 Deer elk caribou normal hosts 0 Cattle 9 dead end hosts o In sheep 9 die 0 Produces melanin pigments tracks black in liver Fasciolopsis buski 0 Common in orient o Endemic regions 60 infection rate in people 0 Found in humans and pigs 0 Largest fluke to infect humans can be 3 in long 0 Fecal contamination of water 0 Ingest metacercaria on aquatic plants 0 Water chestnuts o Bamboo 0 Lotus 0 Water caltrop 0 Host niche GI tract small intestine o Prolific egg producer Clinical Signs F buski 0 Light infection asymptomatic 0 Heavy infection 0 Abdominal pain 0 Diarrhea with mucus I Lots of mucus in feces often 1st indication there is a gut irritation from something 9 could be from a parasite or from something else 0 Interfere with digestionnutrient absorption Pathology Caused by F buski 1 Direct trauma 0 Feed on SI epithelial cells 0 Cause ulcers in muscoa o Interfere with digestion and absorption children 9 hypoproteinenmia 2 Gut obstruction o In very heavy infections can block intestine 3 Immunopathologic allergy to worm products secretedexcreted 0 Has caused fatal anaphylaxis in a few individuals Why a persistant high infection rate in endemic regions 0 Aquatic vegetation economically important 0 Fertilizer used F buski Diagnosis 0 Eggs in feces o Indistinguishable from F hepatica eggs 0 Gut damage and diarrhea Treatment 0 Praziquantel 0 Early and light 9 success 0 Chronic and heavy Prevention 0 Boil veggies for a few seconds before eating 0 Proper disposal of feces Transmission human feces in water Unilocular Hyatid Cyst Growth is endogenouseverything grows within original cyst membrane Cysts get very large quarts of uid and millions of protoscolices Hydatid Sand Multiocular Cyst Really nasty undergoes metatastasis Growth is exogenous grows outward from original cyst lnfiltrates host tissues with numerous daughter cysts Creates large mass that replaces normal organ tissue I I Honeycomb effect in host tissues Cestode development in Definitive host always in the GI tract Metacestode attaches to gut wall Rapid growth to adult size All further growthgtsimply replacement proglottids Adults NO Pathology I In gut mucosa szhyllobotbn39um Ia tum szhyllobotbn um mansonoides Scolex with bothria lst intermediate host 2nd intermediate host Definitive host 2 metacestode forms szhyllobotbn39um Ia tum Distribution worldwide USA great lakes area and west coast Life cycle lSt intermediate host copepodsmall crustacean with procercoid 0 2nd intermediate host freshwater fish including salmon with plerocercoid Definitive host fish eating carnivore humans bears etc Plerocercoid is infective stage for definitive host Adult worms get 1015 m long One of the largest tapeworms known Egg production million per day Eggs operculated can be confused with fasciolid trematode eggs on fecal smear o l2weeks to hatch in freshwater Clinical signs May be asymptomatic 0 May complain of abdominal discomfort o No idea they have it Bothria o prog1ottids o Wider than long broad fish tapeworm o Midventral genital pore No Gut pathology You are the de nitive host pathology Pemicious anemia akamegaloblastic anemia Only in 2 ofthe pop Are genetically susceptible to lack of vitamin B 00 2 Don t produce sufficient intrinsic factor Poorly absorb 132 0 Need vitamin 1312 and intrinsic factorto form EMFgtgtfor normal RBC maturation Not effective in carrying oxygen lam absorbs high unts oan in definitive host worm needs it as a coenzyme gets 90ofhost s supplemented B2 Dx string ofexhausted senile prog1ottids in feces o 0percu ated eggs in feces Rx o praziquantelorNiclosamide o praziquantelkills cells in neck re ion 0 Scolex and prog1ottids pass out intact o Niclosam39de o estroys scolex neck and segments 0 Doesn tkilleg 5 Distrupts worms ability to make ATP prevention o Don t eat raw freshmterfish including salmon Dipagonoporusgradis muulcu o Plerocercoids found in saltvmterfish o shi is made mostly from saltvmter fish especially in Japan Dlpllyllobomium Manson aides aka Spirometm Manson aides o F d 39 southest asia cina Japan Africa andUSA o sparganosis in man organism can live for 10 years 0 parganum common name for p1erocercoid 15 intermediate copepod 2quot int ermediate host fish range ofvertebrates including you Definitive host cats and do gs Procercoid and plerocercoi are infective for humans 5 m 4 fish host cats dogs raccoons Hormonal effect of worm metabolits D mansonm39des Plerocercoids 0 Produce PGF Plerocercoid growth factor I Mimics growth hormone GH I No homology between PGF and GH 0 Human anterior pituitary recognizes PGF as GH Shum down release of GH Connection to Man 0 GH stimulates immune system in man 0 PGF does notgtnegative feedback effect of PGFgtgtno GH PGF causes unrestrained cell growth 0 Stimulates cell growth and causes formation of painful edematous subcutaneous nodules around parasite 0 Can survive years in nodules Homology with cysteine proteinases that hydrolyze collagen 0 Suggest role to facilitate migration in host tissues Man gets this parasite in 3 ways 1 drinking water with infected copepods 2 eating raw or undercooked 2nd intermediate host 3 Application of intermediate host skin frog fish snake onto wounds in flamed eye or vagina Humans have Plerocercoids and are the 2nd intermediate host sparaganum a plerocercoid in tissue of 2nd intermediate host DX lancing nodule and finding parasite Rx surgical removal of infected nodules o Praziquantel as a supplement to make sure all of the worms are gone Prevention don t eat raw or undercooked fish frog legs snake or any flesh that could come from an intermediate host of these parasites l 1 51 0 Cyclophyllidian Cestodes Most of medically important tapeworms Definitive hosts birds and mammals Intermediate hosm mammals Generic life cycle Taeniidae o T291112 Saginaw definitive host 0 T291112 501111111 definitive and intermediate 0 Ecmnococcmgranulosus intermediate 0 Ecmnococcm mult oculanis intermediate Cannot distinguish between eggs 0 All typical taenid type egg 0 Thick striated shell 7291212 301111122 pork tapeworm Distribution worldwide 0 Intermediate host pig and man 0 Infective stage egg De nitive host man 0 Infective stage cysticercus Cestode Mcnasty You can be both hosts 0 Can autoinfect yourself Can distinguish between T 301111122 and T sagmara By the rostellurn hooks and uterine branches in proglottids Man as de nitive host adultsgtGI tract Asymptomatic usually infected ate raw or undercooked pork with cysticerci Pig ingests eggs 0 Food with human feces Cannot be infected by cysticerci How does man get eggs I Retrograde migration of proglottid to upper GI tract 2 Gravid proglottid ruptures in intestine on way out 3 Ingest from environment a Infected individual with poor hygiene b Filth ies pick up eggs from feces No l is really bad massive infection 39gestive enzymes stimulates all the eggs to hatch about 50000 per proglottid Oncospheregtthru gut wallgtto blood vesselsgt cystercerci in any organ No I site Subcutaneous tissuesquot SQ 2quot Site eye Followed by brain heart etc any organ in the body Pathology 0 Tissue location determines severity39 Host produces capsule around parasite Cyst grows for 3 wks Sin dia and stops 0 Creates space occupying lesion in organ 0 Eye 0 Cyst gets larger in the eye thzcmmgywekwm mm mm mama w A mmmwwg 0 mrm m 1 quot infant sgm 39 mm m m waclwlamu an 95mm mm mm wvm uonmm New by m 3m ow I A mm 529 A mamm say and mm ma mm o No capsule produce around it in the anterior chamber 0 Encapsulated by the host in the retina CNS brain and Spinal cord nuerocysticercosis 0 Space occupying lesiongt wide variety of clinical presentations Depends on location and number of cysticerci Seizures Meningitis Encephalitis Pressure necrosis cause pathology Hydrocephaly nuerocgticercosis 1 cause of acquired epilepsy leading cause of epilepsy in children in endemic re ions Sudden onset of adult epilepsy with no family history nuerocysticercosis is a top differential diagnosis 00000000 The incidence of nuerocysticercosis in the USA is higher than suspected being detected by MRI Human as intermediate host39 Parasite down modulate host response to cysticerci Infection can be asymptomatic until parasite dies survives about 2 years Dying parasites can exacerbate the pathology Why They are no longer dampening down modulation the host responses 0 Antigens are released and your body responds Acute local in ammatory reaction highly variable 0 In brain you get most severe manifestations Lesions eventually calcify in tissue DX definitive host with adult in SI 0 Proglottids o Labs be careful Eggs are infective DX Cystercosis 0 Biopsy of lesion especially if SQ in skin Rx Praziquantel albendazole used together 0 Both are cidal drugs so steroids as part of Rx to dampen the in ammatory response to dead parasites especially in the brain 0 Not advised to use Niclosamide kills adulm in GI tract But not the eggs Nor cysticerci in tissues Should give a laxative right before so that the dead worm comes out before the proglottids disintegrate in the body Last stitch effort Prevention and control 0 ommon sources of human infection I undercooked pork I infected food handlers 0 Avoid contamination of food and water with human feces I Good personal hygiene I Proper disposal of human wastes ies transport eggs on feet I ID and Rx infected individuals 0 Properly cook pork I Freezing hard freeze 10C for a week I Treat pigs 0 Can also get it from bear meat Tamra sagl39na ta beef tapeworm Definitive host man 0 Infective stage cysticercus only Intermediate host 0 nfective stage Comment K1iswhat7 Man sheds intact proglottids in feces Adult size 320m Distribution every country where beef is raised Are motile Can actively crawl out of anus Can t be intermediate host Eggs hatch only in digestive tract of cow 0 Oncospheregtgtcysticercus in tissues measly beef contains cysticerci DX proglottids in feces bedding or clothes Rx Prazi or niclosamide Prevention 0 Sanitary disposal of human wastes o Cows are coprophagous love to chow down on human feces T multz39ceps and T serialis Intermediates only Have to ingest eggs Coenurus is infective stage Definitive do s Intermediates herbivorous animals Man accidentally infesting eggs Coenurus form in brain spinal cord eye and muscles Surgical removal if accessible no Rx available OOOOOOOO Echmococcus granulosus Distribution worldwide including US ywhere dogs sheep and man are in close association The smallest tapeworm avg 5mm Scolex neck and three segments immature 1 mature and 1 gravid proglottid I Gravid proglottid disintegrates and eggs go out with the feces 0 Armed scolex with 4 suckers Dog s can harbor 10000s of adulm without clinical effect Definitive hosts dogs and other cani Intermediate host mammalian species usually grazing herbivores get eggs from dog eces Humans are intermediate hosm 0 Must eat an egg to become infected Sylvan cycle sylvan echinococcosis not big threat to most humans Carnivoreherbivore relations 39p o Cycles among wild animals Domestic cycle threat to most humans 0 Usually dogsheep relationship Man accidentally infected from dog feces Humans are dead end hosts EGG O O Hydatid Disease only one that can get very large and under pressure with a lot of fluid Unilocular having a single cell or cavity cysm Each larva becomes hydatid cyst o Secretes 2 layer hyaline membrane 0 protoscolices o Brood capsules Cyst gem large lSqm of uid 0 Under pressure and can rupture Host niche eve here lst most common site liver that s where the blood gem filtered Can really go anywhere I Most common sites in man a Brain bone marrow eye any organ can be infected Viable 20 years Grow slowly o Suppresses host responses to intact cysm Pathology Space occupying lesions Tissue necrosis in organs In braingtgt CNS signs Fluid very antigenic Risk of ruptured cyst o Allergic response to fluid I Ranges from mild to anaphylactic shock o Disseminate infection I Membrane not protoscolices Brood cysts 39 394 1 d tidl c st Liver scans show large hydatid cysm Can develop large lesions with few or no clinical signs associated with them Often hydatid cysm are incidental finding on routine exams or Xrays Calcified cysts from rupture of large hydatid cyst in abdomen One tiny piece of that membranegtgtcan establish another hydatid cyst DX DO NOT BIOPSY hydatid cysm ever I Don t want break off membrane or create a hole for things to leak out Imaging radiographs CAT scans MRI ISA uses hydatid uid as Ag to detect Ab high false negative rate in individuals with intact cysm Why Don t see antibody titers because there is a downplay of the immune response which is suppressed by the parasite Case history association with dogs and sheep or travel to endemic region Rx surgery if cyst is accessible risk associated cyst rupture and anaphylactic shock Albendazole when surgery not possible need prolonged treatment Surgery PAIR technique P puncuter cyst with needle Aaspirate fliud carefully from cyst to decrease pressure I inject protoscolocidal agent to kill parasites and germinal epithelium R reaspirate and remove cyst Intact hydatid cyst almost no host reaction umans unless in location where space occupying lesion creates significant pathology EX brain spinal cord eye bone marrow you would notice these things Why Parasite downmodulation of host responses Prevention Routine deworming of dogs Don t feed raw meat from slaughtered animals to dogs Wash any food you eat raw could be splashed by rainwater containg infected dog feces E mult oculan39s small fox tapeworm Another really nasty parasite but a less chance of being infected than E granulosus Definitive host wild carnivores foxes wolves coyotes infected by eating the cyst Intermediate host wild rodenm such as field mice shrews Infective stage for you is the Egg I Morphology similar to E granulosus Life cycle s1milar E granulosus Distribution N hemisphere Alaska Canada Europe Asia 0 Recent reported cases South Carolina I a Different metacestode form Multiocular hydatid cyst o Daughter cysts bud out from the hydatid making it multiocular Ends up budding so much that the whole organ is compromised I Honeycomb effect Liver is the most common site 0 Cyst buds outward 0 Long slow incubation period 0 Grows like a metastatic tumor I Highly invasive I Very destructive I Membrane pieces can break off and infect another organ I No big uid lled cysts o Humans abnormal host dead end host I No protoscolices I However more likely to break off bits of membrane and spread to other organs in e o y Rx Use surgery then Albendazole to keep it in check hard to get rid of this organism 0 Surgery best option if lesion is accessible I Organ trans t o Albendazole static effect on cyst growth used when the lesion isn t accessible 0 Praziquantelquot DON T USE Not used in echinococcosisquot No protoscolices to kill in multiocular cyst No damage to cyst membrane Appears to enhance cyst growth in experimental animals Prevent 0 Avoid feces from dogs and other canids 0 Don t eat any unwashed fruit especially any that could be contaminated by animal feces 0 Keep dogs regularly dewormed Hmenolepszis Hana dwarf tapeworm a Vampimlepszis Hana Cosmopolitan worldwide ne of the most common tapeworms in humans I Especially children Humans can be the definitive and intermediate host 0 Ingest an e O Gmbee emymereal Definitive man rodenm mm and dnmunata Intermediate Morphology 0 Very small about 1520 inches long 0 Armed rostellum o Shed proglottids disintegrategtgteggs in feces 0 Eggs then walled with polar filaments I not taenid type a Clinical signs asymptomatic o Diarrheaquot really heavy infections and only occurs in children I Autoinfectiongtgtcan produce large infections in children 0 Children are at risk Rx Praziquantel kills both stages Rx children 0 Niclosamide kills adulm but not cysticerciod stages 0 Adultsgtgtinfection is selflimiting I mmunity prevents reinfection Prevention get rid of rodents throw away cereal with grain beetles Hmenolepszis dl39zm39nuta Cosmopolitan Larger Rostellum unarmed Eggs no polar filaments Definitive host Rats humans Intermediate host required 0 Grain beetle plus 90 other arthropod species lnfective stage for definitive host cysticercoids DX Rx and Prevention is the same as for H Hana Family Dilepidiae szylzdiwn caaz39num cucumber tapeworm gravid proglottid looks like a cucumber seed Cosmopolitan Definitive host dog cat man Intermediate host flea eats the egg and gem the cystercercoid lnfective stage cysticercoid Rostellum retractable armed Proglottid 0 Size and shape of cucumber seed 0 2 sew of genital pores 2 sets if both kinds of reproductive organs Proglottids shed intact rice grains an crawl out anus Eggs in capsules called egg packets and they are what the flea larvae eat Proglottids disintegrate 0 Egg packets released 0 Flea larvae eat eggs Definitive host 0 Eat flea with cysticercoids I Get flea guts on hands squashing fleas on pet I Strokes fur with ea gum on it ditto I Dog licks child on face after nipping ea Lesson here Don t squash eas and wash hands after handling pets 0 not the pet it s the ea Order Plagiorcbszrmes Opzlstborcbszrmes 2M intermediate host reguired l Cercaria infect 2n host and encyst 2 Metacercaria found within 2quotd intermediate host Dicrocelium liver ClonorchisOpisthorchis liver Paragonimus lung Nanophytes intestine Heterophyes heterophyes intestine Family Dicrocoeliidae o No aquatic component in life cycle 0 Intermediate snail host terrestrial snail 0 Small eggs 0 Must be eaten by the snail Dicrocelium dendritjcum lancet uke 0 Liver ukegtbile ducts 0 Distribution Eurpoe Asia N Africa N Am and Australia 0 De nitive hosts 0 Herbivores cattle sheep goats cervids 0 RARE in humans but does occur 0 Life cycle 0 2 intermediate hosts 0 Land snail Cronella lubrica usually 0 Common brown ant Formica filsca 0 NO Redia o Infective stage is metacercaria 0 Generic life cycleredia 0 See image online Cercariagtmetacercaria infective stage for de nitive host 1 or 2 cercaria go to the head of the ant brainworms 0 Do not develop further 0 Alter host behavior 0 Ant climbs up and fastens jaws on grass blade 0 Allows ant to be ingested by herbivore Migrating juveniles no trauma to the liver In bile ducts 0 Heavy infection affects liver and gall bladder functions 0 Can impede bile ow to intestine 0 Can interfere with fat digestion o DX eggs in feces 0 False positives in humans eating infected liver 0 To get infected eat an ant o Metacercaria infective stage RX Praziquantel in humans 0 BenXimdazoles in animals Clonorclz15 5111611515 Chinese Liver Fluke Asia 0p15t110r01115 5pp same exact line up as Clonorclz15 Europe and Asia Clonorchis sineusis Chinese Liver Fluke Distribution far east endemic in China Japan Vietnam Korea Taiwan 24 of Chinese immigrants to the USA Host niche bile ducts in liver lSt intermediate host aquatic snail 2quotd intermediate host freshwater sh De nitive host Man Dog cat any sh eating mammal Selffertilize Life cycle all uke cycle stages 0 Metacercaria penetrate the sh 0 Tiny eggs Raw sh most common source of infection Grass carp Light infection asymptomatic Moderateheavegtclinical disease 0 In ammation of bile ducts cholangitis I Outpockets of erosion thru ducts In ammation of pancreas in heavy infections Jaundice heavy infectionsgtbile duct blockage Anorexia and weight loss 0 Diarrhea No problems caused by eggs as long as they stay in the bile ducts OOO Pathology Eggs are very small no host response to eggs in bile ducts Chronic in ammation of bile ducts 0 Adults feeding on epithelium lining and eroding wall of duct Blocked ducts pipe stem brosis Gall stones eggs can be focal point of origin Liver damage I Congestion from backed up bile because of blocked ducts I Granulomas around eggs in liver through erosion in duct wall I Liver necrosis cells surrounding granuloma In ammation of gall bladder and pancreas can occur Cholangiocarcinoma of bile ducts I Common cancer in uke endemic regions I Clonorchis and Opisthorchis both I Flukes induce metaplasia in bile duct epithelium 000 00 I Metaplasia becomes neoplasia formation of tumors Pipestem brosis around bile ducts in the liver Eggs and ukes that get into the liver from bile duct erosion and cause granulomas and loss of liver function 0 Very heavy infectiongtgtcirrhosis of the livergtgtloss of normal liver function 00 DX eggs in fecal sample RX Praziquantel Prevention difficult Farm raised fish grass carp served raw as a delicacy Most common source fish farming where fertilizer is human waste Nothing but cooking will kill the metacercaria Not pickling salting drying or smoking Paragom39mus westelmam39 human lung uke Coffee Bean uke oriental lung uke Distribution Japans China Korea Vietnam Thailand Cambodia India Asia Micronesia Philippines Numerous reservoirs Zoonosis Host niche lungs 0 Live in pairs 0 Cross fertilize I Hermaphrodites Genetic variations 0 Diploid I Pair up in cyst in lungs I Cross fertilize I No pairinggtno cyst formation 0 Triploid considered more pathogenic I Form cysts without pairing upgtgtrelease eggs I Always form cysts I Parthenogenic can t form sperm Coffee bean uke o lst intermediate host aquatic snail fast streams 0 2nd crustaceans crabs crawfish o Definitive host Man and other mammals any mammal that will eat crustaceans 0 Eggs 0 Coughed upgtout in bloody sputum o Coughed up and swallowedgtout in the feces Water essential for eggs to hatch 2 wks until hatches MiracidiumgtSporocystgtRediagtCercariagtMetacercaria metacercaria encyst in viscera and mussel of crustacean Clinical disease severity dependent upon parasite load 0 Coughgtbloody sputum with eggs in it Pleural pain Dyspnea Severe casesgtgtpleural effusion accumulation of fluid in pleural cavity Radiographs signet ring lung lesion could me misdiagnosed as TB 0 O O O anamna uxktaml ul nanenatmutwau rMiinles across h omin mm o dlipmaim pammmnta pleural an u up were menace ima Ilmx Iissue EEES mama up and mumquot a swallowed to 20 am in fans Paragonimus westermani 343quot 2 33321 l Numan naesl widenMY A anmmtaw A gamma an M Aeuuamne Asotuaesaesuae Pathology Lung lesions called pseudotubercles Mlgatmgjuvemles no Immune reac Ion Hostcesponse adults form 1ung cysts eggs pass out up bronchloles Lung abscess develo cnent o Can get a bactena1 secondary Infection Chrome tn acncnatory ukes o nulomaformauonar dcystwnn ukepan o Fxbrous capsule forms eggs trapped a1so o anuloma formauon around eggs tn 1ung ttssues Abscesses nea1 slowl o B come calcx ed as adults at o Consequence lots of 1ung fxbroses o Eosmophlhamlungs O t t 1estons can be fata1 Fata1 cardlac cases thnp We ermamreposted Usua11ycesu1ts of very heavy Infectionquot Transmxssxon o Eatmg raw orundercooked crustaceans o Raw crustacean Jutce cleantng crabs o chk ng ormarmatmg tn Wme vmegar orbnne does notklll cnetacercana 0 DON T EAT RAW austaceans Louxsxana connectxon P kellicotti O O O O 2quotd host common crawf1sh we lover to eat Biology and pathogenesis DX I Rule out tuberculosis I Rule out other causes of lunch abscess I Eggs in sputum and or feces I ELISA I Rapid intradermal test Paragom39mus antigen under skin china used on 2 million people 20 infected RX Praziquantel gets the en all I out the lungs and everywhere else Nanopbyteus salminocola 0 00000 00 O O salmon poisoning elkomin uke fever Associated with eating raw salmon Disease causing agent a rickettsia Neorickettsia belm39ntboeca Antibiotic will cure the bacterium because it is the cause of the disease Salmon poisoning affects dogs I High fever with purulent discharge from eyes I Vomiting and diarrhea I If untreated 90 mortality in dogs I Disease is milder in humans 0 Vomiting and Diarrhea o Anorexia and weight loss Life cycle Egggtmiracidiumgtrediagtcercariagtmetacercariagtadult NO SPOROCYST lst intermediate host aquatic snail I No sporocysts 2quotd intermediate host of uke freshwater fish and salmon Definitive hosts fisheating birds and mammals including humans Host niche small intestine no pathology associated with the uke itself 0 Heterapbyes Izeterapbyes Metagom39mus yokaga wai Tiny ukes 1mm long tear shaped Intestinal ukes small intestine Common in Africa Asia Middle and Far East endemic in certain parts of Egypt All species considered potential human pathogens e cycle generic 1 intermediate host aquatic snail 2 d intermediate host freshwater is Def1nitive host humans fish 39 l eating anima s Clinical disease gastric distress fatigue malaise diarrhea Pathology 0 Mild in ammation at site 0 Heavy infection mucosal damage and potential for ectopic parasite locations so tiny gets into blood and is disseminated failure cases in Philli ines Cayenne Demuala me am of rushmama mm nsh m encysi as melacemavue m m 15m 71 m r 39 xAA xk amp MW e 9mm rxlxk 9 mu mm mm em muswia emerge hum vk Egg and penallnte ma mm mm JV Sumac m m m mi lissu Dx eggs in feces resemble C sinensis eggs Rx Praziquantel B b mm 3 9 n mung m m was can missed a well mm mm mch mgzmm unduwnke mung mehnewa 26W a ammnl be em M4 0 lull rdeve are paxszd a eggs em with tom mramdmm n mg Mm lmwwd d we wwavax Mahayana mm 6 m we small inlellme 0 Mull m small mmwie A s mm 5va K magnum Slag Fatalities associated with Valve and muscle damage by parasite in heart 15 of cardiac Parasites that Require 2nd intermediate host 0 Cercaria 9 infect 2nd intermediate host and encyst Metacercaria 9 within 2nd intermediate host 0 Must eat 2nd intermediate host to get infected Family Dicrocoeliidae o No aquatic component in life cycle Terrestrial snail Small eggs that must be eaten by snail host Dicrocoelium dendriticum lancet fluke 0 Liver flukes 9 bile ducts 0 Distribution Europe Asia North Africa North America 0 Definitive hosts herbivores cattle sheep Life cycle 2 intermediate hosts 0 15 land snail Cionella lubrica in US 0 2 common brown ant Formica fusca Selffertilize General life cycle stage excluding redia stage Cercaria 9 metacercaria o Infective stage for definitive host 0 1 or 2 cercaria 9 head superior ganglion ofant 0 Don t develop further 0 Produce molecules that alter host behavior Parasite manipulation of host 9 no uncommon in parasite infections How Dicrocoelium dendriticum alters host behavior 0 Ant climbs up and fastens jaws on grass blade at dusk temperature drops 0 Ant can t unlock jaws until morning when sun comes up temperature rises o Increases chances ant will be ingested by herbivore o Allows parasite to complete life cycle In Definitive Host 0 Metacercaria excyst 9 migrate to common bile duct 0 Migrating juveniles no trauma to liver o In bile ducts inflammation and fibrosis 0 Heavy infection affects liver and gall bladder functions 0 Can impede bile flow to intestine 0 Can interfere with fat digestion Diagnosis of Dicrocoelium dendriticum 0 Eggs in feces o Fals positives in humans eating infected liver 0 To get infect must eat an ant o Metacercaria infective stage 0 Treatment 0 Praziquantel in humans 0 Benzimidazoles in animals Clonorchis sinensis Chinese liver fluke 0 Distribution endemic in China Japan Vietnam Korea 0 25 of Chinese immigrants to US are infected 0 Host niche bile ducts in liver 0 1st H aquatic snail o 2quotd H freshwater fish 0 Definitive host man dog cat fisheating mammal o Selffertilize 0 Life cycle all fluke stages 0 Eggs9 miracidium9 sporocyst 9 redia 9 cercariea 9 metacercaria Clinical Signs 0 From eating raw freshwater fish most common source of infection 0 Light infection asymptomatic o Moderateheavy infection 9 clinical disease 0 Inflammation of bile ducts o nterferes with liver function 0 Anorexia and weight loss 0 Diarrhea Pathology 0 Eggs are very small and get no host response when in bile ducts 0 Chronic inflammation of bile ducts 0 Adults feeding on epithelium lining and eroding wall of duct 0 Blocked bile ducts pipe stem fibrosis 0 Chronic damage leads to thickening of walls and obstruction of duct 0 Gall stones can form 0 Liver damage heavy infections 0 Congestion from backed up bile because of blocked ducts o Granulomas around eggs in liver 0 Liver necrosis cells surrounding granuloma can die 0 Inflammation of gall bladder and pancreas via retrograde infection 0 Cholangiocarcinoma bile duct cancer 0 Common cancer in fluke endemic regions 0 Clonorchis and Opisthorchis o Flukes induce metaplasia in bile duct epithelium o Metaplasia 9 neoplasia Diagnosis and Treatment 0 Eggs in fecal sample 0 Praziquantel 0 Prevention difficult o Pickling salting drying smoking will not kill metacercaria 0 Most common source fish farm raised 0 Grass carp o Fertilizer is human waste Paragonimus westermani in US P kellicotti 0 Distribution japan china korea philippines asia india 0 Numerous rservoirs zoonosis 0 Host niche lungs 0 Live in pairs in lung 9 crossfertilize 0 Genetic variations 0 Diploid pair up and form cysts in lungs cross fertilize no pairing 9 no cyst formation 0 Triploid considred more pathogenic always form cysts parthogenic can t form sper Coffee Bean Fluke Paragonimus westermani 0 1st H aquatic snail in fast streams o 2quotd H crustaceans crabs and crawfish o Definitive host man and other mammals any that eat crustaceans Morphology o All stages in life cycle 0 Egg coughed up in bloody sputum or out in feces if swallowed 0 Water essential for egg to hatch 0 Life cyle egg 9 miracidium 9 sporocyst 9 redia 9 cercaria 9 metacercaria o Cercaria knoblike tail can t swim o Creep along bottom and penetrate crustaceans o Encyst as metacercaria in vescera and muscle Clinical Disease 0 Cough 9 bloody sputum with eggs in it o Often misdiagnosed as TB 0 Pleural pain 0 Dyspnea difficulty breathing 0 Severe cases 9 pleural effusion accumulation of fluid in pleural cavity 0 Radiographs signet ring lung lesion Pathology for Paragonimus westermani 0 Lung lesions called quotpseudotuberclesquot 0 Host response 9 adults from lung cysts each pair creates necrotic lesion around pair 0 Eggs pass out up bronchioles o Lungs abcess development leads to bacterial secondary infection 0 Heal slowly 0 Become calcified as adults die 0 Consequence lots of lung fibrosis IgE and IgE antibodies not protective 9 parasite produces enzymes that chop the 0 antibodies apart 0 Chronic inflammatory response to flukes o Granuloma formation around cyst with fluke pair 0 Will communicate with bronchioles o Fibrous capsule forms around cyst o Granuloma formation around eggs in lung tissues 0 Eosinophilia in lungs 0 Can go to brain heart other ectopic locations during migratory period lesions can be fatal 0 Fatal cardiac cases reported 0 Usually result of very heavy infection Transmission 0 Eating raw or undercooked crustaceans 0 Raw crustacean juice from cleaning 0 Pickling or marinating in wine vinegar or brine doesn t kill metacercaria Paragonimus kellicotti o 2quotd host crawfish 0 Biology and pathogenesis same as P westermani Diagnosis for Pulmonary paragonimiasis 0 1st have to rule out TB 0 Eggs in sputum andor feces o ELISA antigen capture 0 Rapid intradermal test Paragonimus antigen under skin Treatment Praziquantel gets all from lungs and elsewhere salmon I u 0 Associated with eating raw salmon 0 Disease causing agent rickettsia from Neorickettsia helmintoeca 0 Only time cause is not parasite actually bacteria on this parasite o If parasite doesn t have bacteria there will be no complications 0 Antibiotics will cure because bacterium causes disease 0 Salmon poisoning affects dogs 0 High fever with purulent discharge from eyes 0 Vomiting and diarrhea o If untreated most die 0 Disease is milder in humans 0 Vomiting and diarrhea o Anorexia and weight loss Life Cycle egg9 miracidium redia cercaria metacercaria adult No of intermediate host required Life cycle NO SPOROCYSTS 0 1st IH aquatic snail o 2quotd H freshwater fish and salmon o Definitive hosts fisheating birds and mammals including man 0 Host niche small intestine burrow into wall between villi o No pathology associated with fluke itself II l I I I VI 1 I in U I I I C 0 Tiny flukes 1 mm long tear shaped o Intestinal flukes small intestine 0 Common in Africa Asia Middle and Far east 0 Endemic in certain points of Egypt 0 All species considered potential human pathogens 0 Life cycle general fluke cycle 0 1st intermediate host aquatic snail 2quotd intermediate host fresh or brackish water fish mullet Definitive host fisheating birds and mammals Burrow into SI wall between villi 000 Clinical Disease 0 Gastric distress fatigue malaise diarrhea 0 Pathology 0 Mild inflammation at site 0 With heavy infection burrowing into SI wall causes mucosal damage and potential for ectopic parasite location so tiny both adults and eggs can get into blood and become disseminated brain heart etc Fatalities associated with valve and muscle damage by parasite in heart 15 of cardaci failure in Phlippines 00 DX eggs in feces resemble Chlonorchis sinensis eggs Rx Praziquantel Platyhelminthes Cestodes quottapewormsquot 0 Unique to Cestodes 0 NO digestive system 0 Niche always intestinal tract in definitive host 0 N0 pathology to gut mucosa in de nitive host adhesion not invasion 0 Two orders of Cestodes o Pseudophyllidian o Cyclophyllidian o Differ in I Type of scolex hold fast structures I Onchosphere and metacestodes forms Proglottids segment that has both sets of reproductive organs Strobila long chain of proglottids 0 Growth is from anterior to posterior Tapeworm is basically a huge collection of individual reproductive units Scolex contains quotholdfastquot organs 0 Suckerlike organs 0 AcetabulumCyclophyllidian o slitlike o BothriaPseudophyllidian Rostellum domed shaped area on end of scolex o Protrudes 0 Armed with hooks o Unarmed without hooks o Taenia saginatta doesn t have one Neckbetween scolex and 1st proglottid in strobila 0 Contains stem cells 0 Give rise to new proglottids 0 Kill neck tissue to kill the worm Tegument covered in microvilli microtriches 0 Functions 0 Absorption all nutrition absorbed through surface 0 Excretion waste products of metabolism osmoregulation have to control water balance Glycocalyx outermost covering of tapeworm o Composed of mucopolysaccharides glycoproteins 0 Function protection against digestive enzymes in gut Calcareous corpuscles structures in cestode tissue Have nervous and muscular system 0 Each proglottid has nerves 0 Shed proglottids quotcrawlquot around Reproduction Hermaphroditic o Monoecious 0 Has 1 or 2 complete sets of male and female reproductive organs per proglottid 0 Generally 1 ovary 1 uterus at least 2 testes 0 Don t selffertilize within each segment 0 Fertilization occurs in mature proglottids next to each other 0 Sperm transferred between mature proglottids which lie next to each other Gravid proglottid uterus filled with thousands of fertilized eggs Egg zygote o Pseudophyllidian thin shelled and operculated tied to water 0 Cyclophyllidian dipylidium thin shelled taenid thick schelled How are eggs released 0 Gravid proglottid shed intact in feces 0 Ex Taenia spp o Gravid proglottid disintegrates as shed 9 eggs out in feces 0 Ex Hymenolepsis spp 0 Eggs shed thru uterine pore and out with feces 0 Later chain of empty senile proglottids out in feces 0 Ex Diphyllobothrium spp Life Cycle of Cestodes 0 Egg 9 onchosphere 9 metacestode 9 adult 0 Onchosphere larvae in egg hexacanth meaning 3 pairs of hooks o Metacestode juvenile forms of tapeworm 0 Always in intermediate host 0 Always extraintestinal 0 Adult in intestinal tract in definitive host ALWAYS Pseudophyllidian o Onchosphere coradicium o 2 metacestode forms 0 1st is procercoid o 2quotd is plerocercoid Cyclophyllidian o Onchosphere hexacanth larva o 1 metacestode form 0 Different versions I Cysticercoids 39239 Cysticeroid 39239 Tetrathryidium I Cysticercus 39239 Coenurus 39239 Hydatid cyst unilocular and multiocular forms Pseudophyllidian Life Cycle 0 Has aquatic component 0 Egg 9 quot39 9 r quot9 39 quot9 adult tapeworm o F 39 quot fmc 39 39 39 I 39 ciliated and must be eaten by 1st intermediate host 0 2 metacestode forms 0 Procercoid in 1st H I Coricidum 9 penetrates though gut 9 into tissues I 3 paris of hooks that aid in penetration 9 procercoid I Has cercomer o Plerocercoid in 2nd H I Procercoid aided by 3 pairs of hooks in cercomer penetrates gut 9 into muscle 9 plerococoid I Infective stage for definitive host I Has scolex and short strobila formation I True juvenile cestode Cyclophyllidian Life Cycle 0 Egg 9 onchosphere hexacanth 9 cystercoid type in IH 9 adult 0 Egg hexacanth 9 onchosphere 9 cysticercus type in IH 9 adult Cysticercoids solid cyst or bladder membrane bound sack single inverted scolex Cysticercus fluidfilled cyst or bladder membrane bound sack 0 Single inverted scolex o Membrane of cyst is germinal tissue that gave rise to scolex Coenurus fluidfilled cyst with several inverted scolices each on a stalk Hydatid cyst a Unilocular 0 Growth is endogenous 9 everything grows around original cyst o Cysts get very large 0 Fluid is under pressure 0 Daughter cysts develop inside cyst b Multiocular 0 Really nasty 9 undergoes metastasis 0 Growth is exogenous 9 growth is outward from original cyst o nfiltrates surrounding host tissues with numerous daughter cysts 0 Growth replaces normal organ tissue and destroys it I Doesn t fill with fluid under pressure Cestode Development in Definitve Host 0 Always in GI tract 0 Metacestode attaches to gut wall 0 Rapid growth to adult size 0 All further growth 9 simply replacement proglottids 0 Adults no pathology to gut mucosa no damage by adults Pseudophyllidian o Holdfast organ bothria lateral grooves Diphyllobothrium latum broad fish tapeworm o Largest tapeworm to infect humans 0 Distributionworldwide o In US Great Lakes area and west coast 0 Life cycle 0 1st H copepod with procercoid o 2quotd H freshwater fish salmon with plerocercoid o Definitve hosts fisheating carnivores 0 Dogs cats humans bears foxes mustelids pinnepids o Plerocercoid is infective stage for definitive host 0 Adult worms get 1015 meters long 0 One of largest tapeworms known 0 Egg production 9 million eggs per day 0 Eggs operculated can be confused with trematode eggs on fecal smear o Takes about 912 days to hatch 0 Clinical signs 0 May be asymptomatic 0 May complain of abdominal discomfort o Proglottids wider than long 9 broad fish tapeworm o Genital pore right over uterus because eggs are released as they are produced I In center of proglottid Plerocercoids are not microscopic visible No gut pathology humandefinitive host Pathology in Specific Group Pernicious anemia aka Megaloblastic anemia 0 Only in 2 of population 0 2 are genetically susceptible to lack of vitamin 312 0 Don t produce Need vitamin BIZ and intrinsic factor to form EMF 9 for normal RBC maturation D latum o Absorbs hhigh amounts of 312 in definitive host 0 Worms needs it as coenzyme in metabolic pathway 0 Absorbs 90 of host s orally supplemeted 312 0 Doesn t cause underlying problem 9 just exacerbates it D latum Diagnosis and Treatment 0 Dx string of exhausted senile proglottids in feces o Operculated eggs in feces 0 Tx Praziquantel or Niclosamide o Praziquantel kills cells in neck region scolex and proglottids pass out intact o Niclosamide kills cells in neck region destroys scolex neck and segments by destroying the glycocalyx allowing digestive enzymes to attack tegument of worm I Doesn t kill eggs in gravid proglottids Prevention 0 Don t eat raw freshwater fish Diplogonoporus grandis o Whales definitive host and humans 0 Shorter Diphyllobothrium mansonoides 0 Distribution China Asia Africa USA 0 Sparganosis in man 0 Sparganum common name for the plerocercoid o Organism can live for 10 years in man as 2nd H 0 Hosts 0 1st H copepod possibly 0 2quotd H fish vertebrates including humans 0 Definitve hosts cats and dogs 0 Life cycle egg 9 coracidium 9 procercoid 1st H copepod tadpole 9 plerocercoid 2nd Hfish frog snake bird mouse man 9 definitive host domestic and wild cats dogs raccoons o Humans are 2nd H 0 Dead end host because nothing eats us Hormonal Effect of Worm Metabolites o D mansonoides plerocercoids 0 Produce PGF plerocercoid growth factor 0 Mimics human growth hormone o No homology between the 2 0 Human anterior pituitary recognizes PGF as growth hormone o Shuts down release 0 What is connection for man 0 Growth hormone has some stimulation on immune system in man 0 PGF does not 9 negative feedback effect of PGF 9 no growth hormone 0 Aids parasite in evasion of host immune defenses What would benefit parasite with PGF in 2nd IH 0 Causes unrestrained cell growth in other 2quotd H 0 Causes tissue surrounding plercoercoid to form an endematous and painful nodule in humans 0 PGF has homology with cysteine proteinases that hydrolyze collagen o Mimics mammalian growth hormone GH I Has component that allows it to react with mammalian GH receptors I No homology between PGF and GH no evolutionary relationship 0 Human and other mammalian anterior pituitary recognizes PGF and GH I Negative feedback to anterior pituitary gland9will shut down production of GH Man enters parasitic cycle by 3 ways 1 Drinking water with infected copepods 2 Eating raw or undercooked 2nd H 3 Application of intermediate host skin 0 Frog fish or snake onto wounds inflamed eye or vagina o Are thermotactic o Definitve host warmblooded Humans have plercoercoids in tissues 9 we are 2md H Cyclophyllidian Tapeworms 0 Most of medically importance 0 Definitve hosts birds and mammals 0 Intermediate host mammal 0 Life cycle egg 9 39 9 39 or 39 quottype 9 adult Taenid tapes are of the most medical importance and economic significance Taenia saginata humans can be only definitive host Taenia solium mcnastyquot can autoinfect yourself because can be both definitive and intermediate host Taenia saginata 0 Distribution where beef is raised 0 Definitive host human infective stage cysticercus 0 Intermediate host herbivore 9 mostly cattle infective stage egg 0 Eggs only hatch in digestive tract of definitive host 0 Humans shed intact proglottids in feces o Proglottids are motile 0 They actively crawl out anus at night 0 Causes measly beefquot 9 contains cysticerci T saginata Clinical Signs 0 Asymptomatic no gut pathology 0 Diagnosis proglottids in feces bedding or clothing in morning 0 ELISA detecting worm antigen 0 Treatment Praziquantel Taenia solium Cestode Mcnasty o Distributionworldwide 0 Intermediate host pig infective stage egg 0 Definitve host cysticercus infective stage cysticercus 0 Most dangerous tapeworm to humans 0 Can be both definitive and intermediate hosts 0 Can reinfect yourself 0 Can autoinfect yourself 0 Life cycle for definitive host same for saginata but with a pig instead of a cow 0 Man as definitive host adults 9 GI tract 0 Asymptomatic usually 0 Infected by eating raw or undercooked pork with cysticerci o Pig ingests eggs 0 Life cycle for intermediate host now have cysticerci in body 0 Onchospheres can go anywhere in the body ex brain eye muscle How does man get the eggs 1 Retrograde migration of proglottid to upper GI 0 Reverse peristaltis from vomiting 0 Administration of pergatives 2 Gravid proglottids rupture in intestine on way out 9 autoinfection 3 Ingest from environment 0 Infected individual with poor hygiene o Filth flies pick up eggs from feces Massive infection digestive enzymes stimulate all eggs to hatch about 50000 per proglottid Distinguish between T solium and T saginata o Rostellum hooks uterine branches in proglottids o T solium less than w4 side branches on each side of uterus o T saginata 1520 branches Onchosphere 9 thru gut wall 9 blood vessels 9 cysticerci in any organ Number 1 site subcutaneous tissies 2quotd site eye 0 Followed by brain Pathology 0 Tissue location 9 determines severity seen clinically 0 Host produces capsule around parasite o Cyst grows for 3 weeks and stops 0 Creates space occupying lesion in organ o In eye 0 Cause irreparable damage to retina o Cyst gets larger in eye 0 Protected from host immune response I Prevents damage by immune response 0 NO capsule produced around it o In CNS brain and spinal cord 9 neurocysticercosis 0 Space occupying lesion wide variety of clinical presentations I Depends on location and number of cysticerci o Seizures meningitis hydrocephalus encephalitis pressure necrosis I Hydrocephaly caused by cysticercus blocking ventricle I Calcification of older lesions I Pressure necrosis irreversible damage caused by growth of cysticercus o Neurocysticercosis number 1 cause of acquired epilepsy I Leading cause ofepilepsy in children in endemic regions 0 Sudden onset of adult epilepsy with no family history I Neurocysticercosis should be at top of the list Parasite down modulates host response to cysticerci 0 Infection can be asymptomatic until parasite dies survive about 2 years 0 Dying parasites can exacerbate the pathology 0 No down modulation anymore 0 Release antigens that initiate inflammatory and immune responses 0 Acute local inflammatory reactions highly variable o In brain most severe manifestations 0 Can be clinically significant brain and eye 0 Lesions cysticercus eventually calcify in tissue T solium Diagnosis and Treatment for def host with adult in SI 0 Proglottids o Labs must be careful o ELISA antigen capture in feces o Cysticercosis 0 Biopsy of lesion especially if SQ meaning skin 0 Neurocysticercosis I Imaging CT MRI I ELISA antibody capture 0 Treatment Praziquantel Albendazole 9 DOC 0 Both are cidal drugs so steroids also added to dampen inflammatory response to dead parasites especially in brain 0 Niclosamide kills adults in GI tract but not eggs or cysticerci in tissues I Not widely used Prevention and Contol 0 Avoid contamination of food and water with human feces o Properly cook pork 0 Freezing 10 C for a week 0 Treat pigs Other Taenids 9 T multiceps and T saerialis o Infective stage coenurus o Definitive hosts dogs and other canidae 0 Intermediate hosts herbivorous mammals 0 Man accidentally infecting by ingesting eggs 0 Humans intermediate host 0 Coenurus form in brain spinal cord eye and muscles 0 No treatment available Echinococcus granulosus o Smallest tapeworm o Scolex neck 3 proglottids o Definitive host dogs and other canids 0 Intermediate hosts mammalian species 0 Also humans 9 must eat egg 0 Humans are dead end host 0 Has rosteum with hooks o Produces uniocuar cysts 0 Each larvae becomes hydatid cyst I Secrete 2 layer membrane I Secrete hyaline membrane I nner layer germinal epithelium I Protoscolices I Daughter Brood capsules 0 Cyst can get large eg 15 quarts of fluid I protoscolices o Cyst gets large ex 15 qts of fluid I Under pressure and can rupture 0 Host niche everywhere 0 15 liver and 2quotd lung 0 Any organ can be infected 0 Common sites brain bone marrow eye 0 Grow very slowly viable for 20 years 0 Suppresses host responses to intact cysts 9 no eosinophilia Sylvan cycle 9 among wild animals Domestic cycle 9 usually dogsheep relationship 0 Threat to most humans 0 Man accidentally infected from dog feces E granulosus Pathology 0 Space occupying lesions 0 Tissue necrosis in organs o In brain 9 CNS signs 0 Fluid very antigenic 0 Risk of ruptured cyst 1 Allergic response to fluid o v Range from mild to anaphylactic shock 2 Disseminate infection 39239 Membrane not protoscolices E granulosus Diagnosis 0 Never biopsy hydatid cyst 0 Imaging radiographs CTscan MRI 0 ELISA uses hydatid fluid as antigen to detect host antibodies 0 High false negative rate in individuals with intact cysts o Parasite down modulates immune response Treatment 0 Surgery if cyst is accessible 0 Pair technique I Puncture with needle aspirate carefully to decrease pressure inject to kille parasites reaspirate and remove cyst o Albendazole when surgery is not possible 0 Require prolonged treatment Intact Hydatid cyst 0 Almost no host reaction in humans unless in location where space occupying lesion creates significant pathology 0 Ex brain spinal cord eye bone marrow 0 Why 0 Parasite downmodulation of host responses 0 If cyst ruptures antibody titers rise eosinophilia occurs Host response is reaction to host cells dying Prevention 0 Routine deworming of dogs 0 Don t feed raw meat from slaughtered animals to dogs 0 Wash any food you eat raw Echinococcus miltiocularis small fox tapeworm o Definitive host wild carnivores foxes wolves coyotes 0 Intermediate host wild rodents o Humans are intermediate hosts 0 Egg must be ingested 0 Get hydatid cyst stage 0 Don t produce of protoscolices because we re dead end host 0 Distribution northern hemisphere o Multiocular hydatid cyst 9 different metacestode form Liver most common site 0 Cyst buds outward like metastatic tumor 0 Grows slowly 0 High invasice 9 destroys normal tissue 0 Membrane pieces can break off 0 No big fluid filled cysts E mutiocuaris Treatment 0 Surgery is best option if lesion is accessible organ transplant 0 Albendazole 9 static effect on cyst growth doesn t kill it but prevents it from budding out o Praziquantel doesn t inhibit cyst growth 0 No protoscolices to kill in multiocular cyst 0 Causes no damage to cyst membrane 0 Appears to enhance cyst growth in experimental animals Prevention 0 Don t eat unwashed fruit 0 Keep dogs regularly dewormed Family Hymeolepiddae o Hymenolepsis nana and H diminuta 0 Distribution worldwide 0 Both innocuous o Metacestode stage cysticercoids 0 Intermediate host is optional for H nana 9 autoinfection o No clinical signs because barely penetrates gut wall 0 H dimunta 9 H required grain beetle and arthropods Clinical signs 0 Asymptomatic 0 Only small children may have diarrhea Treatment 9 Praziquantel kills both stages o In adults infection is selflimiting o Immunity prevents reinfection Prevention get rid of rodents and don t eat food with grain beetles Dipylidium caninum o Definitive host dog cat man 0 Intermediate host flea o Infective stage cysticercoids o Proglottids shed intact 9 rice grains o In proglottid eggs in capsules egg packets o Proglottids disintegrate 0 Egg packets released 0 Flea larvae eat it Definitive host must ingest cysticercoids 0 Eat flea with cysticercoids 0 Get flea guts on hands 0 Strokes fur with flea guts on it 0 Dog licks child on face after nipping flea It s not the pet it s the flea o Rostellum retractable armed and multiple rows of hooks o Proglottids 0 Size and shape of cucumber seed Reproductive organs 2 male and 2 female Double genital pores bilateral Proglottids shed intact I Out with feces rice grainsquot I Crawl out anus 0 Eggs in capsules quotegg packetsquot I 815 eggs within each 0 Proglottids disintegrate in environment I Eggs packets released I Flea larvae eat D caninum eggs OOO SAME AS ABOVE Dupicate 2 each sets of both reproductive organs Double genital pores each side of proglottids Proglottids disintegrate eggs in packets in environment Flea larvae love to eat the eggs of this tape 0000 Life Cycle Picture Definitive Host Eats flea with cysticercoid OR Gets flea quotgutsquot on hands when squashing fleas on pets OR Strokes fur with flea guts on it OR Dog licks child on face after nipping flea Lesson here don t squash flea between your fingernails AND wash hands after handling pets not the pet it s the flea No clinical disease Possible mild abdominal discomfort 0 Usually after people find proglottids DX finding proglottids llrice grainsquot in stool clothing bedding Rx Praziquantel pets and people Niclosamide pets Nematodes Helminths Phylum Nematoda o Nematodes or llround wormsquot Most freeliving and nonpathogenic Found everywhere soil saltwater freshwater Most are very host specific OOO Caenorhabditis elegans 0 Free living 0 Entire genome sequenced 19080 genes Trichenella spiralis o Parasitic o More DNA in genome Seem to need more DNA to be parasitic General Nematode Morphology 0 Round and nonsegmented 0 Round and tapered at both ends Bilaterally symmetrical Body wall Cuticle Hypodermis Body wall musculature Pseudocoelom a body cavity Complete GI tract Cuticle outer layer 0 Structure and composition unique to each species Acellular layers of proteins lipoproteins collagen Lines all external openings buccal cavity esophagus excretory pore vagina Function protection resistant to chemicals OOO Alae lateral thickenings of cuticle o No function with respect to pathology 0 Simply an ID key Well developed muscular system 0 Muscle with same kind of contractile filaments as humans Well developed nervous system 0 Some of major neurotransmitters same as humans o Sensoryorgu 39 r and quot r I Papillae I Amphids I Phasmids o Pseudocoelom o Fluid filled body cavity filled with hemolymph quotHydrostatic skeletonquot of the worm NW quot39 fluid in 39 39 Longitudinal muscles 000 0 Complete GI Tract simple tube o No stomach no muscle layers in intestinal tube 0 Buccal cavity mouth 0 Esophagus I Muscular I Enlargements called quotbulbsquot I Glands aid digestion o Intestine I No peristaltic action I All pushing of digestion is result of esophagus taking more food and pushing the rest down I Lined with columnar cells with microvilli I Nonmuscular o Anus I quotDepressor aniquot muscle 0 Lips o Ascarids typically 0 Buccal cavity 0 Lined with cuticle o Ormaments called quotteethquot or quotplatesquot Hookworms only ones we ll look at o Secretionexcretion o Secretion fluids out an excretory pore o Excretion solid wastes out an us 0 Reproductiondioecious 0 Some females 9 ovoviviparous eggs retained hatch within larvae released 0 Most oviparous release eggs 0 Rare parthenogenic female worm produces both male and female offspring o Sexes must find each other for mating to occur 0 Females usually larger than males 0 General life cycle egg embryonated 9 ll 912 913 9 J4 9 adult 0 Stages separated by molting total of 4 molts 0 Rule of thumb infective stage is 13 o Hyphobiosis arrested development I Parasite goes formant during development in host tissues I Enhances survival and completion of life cycle of parasite Neglected Tropical Diseases NTDs 0 Chronic and disabling infections endemic in underdeveloped regions especially rural regions o Povertypromoting because of their impact on 1 Soil Transmitted Helmiths STH 0 Include most common neematods in humans 0 Rounds whips hooks o Unholy trinity of STH 9 Ascaris Trichuris Ancyolstoma necator 0 Also include Strongyloides Trichuris trichiura whip worms 0 Distribution worldwide areas with poor sanitation 0 3rd most common nematode in man 0 Prehistoric ancestors 9 eggs seen in coprolites 0 Direct life cycle 0 Children get heaviest infections 9 STH o Morphology 0 Thick posterior region thin anterior end 0 Stichosome esophagus lined with stichocytes gland cells 0 Viable 2 years 0 Host niche large intestine o STH requires warm moist shady soil to develop 0 Life cycle 13 first hatches out in small intestine then eventually molts into JS adult which is then carried to large intestine 0 Females produce 30005000 eggsday Clinical Disease of T trichiura 0 Less than a 100 adults are asymptomatic 0 Over 200 have clinical disease 0 Acute dysentery heavy initial infection 9 in children 0 Diarrhea with blood and mucus o Anemia 0 Weight loss and growth retardation 0 Severe inflammation of gut mucosa I Protracted tenesmus straining to defecate I Rectal prolapsed medical emergency 0 Chronic colitis slow build up of parasites o Inflammatory bowel disease 0 Malnutrition o Anemia O Retarded development physical and mental I Can be seen with moderate infections in children Pathology of Whip Worms Trichuris trichiura o Invade mucosa and feed on host tissues in gut 0 Tissue trauma 9 capillary damage 9 hemorrhage some 9 anemia 0 Local inflammation of gut mucosa o Edema 0 Increased inflammatory cells into gut o Interferes with nutrient absorption Clinical signs may suggest amebiasishookworm infections Diagnosis fecal sample 0 Bipolar eggs look like footballs o Colonoscopy reveals adults Treatment 0 Mebendazole o Albendazole o If in doubt about diagnosis treat anyway Prevention of T trichiura o Sanitation 9 proper disposal of feces 0 Don t use human feces as fertilizer o Prevent contamination of dirt where children play 0 Reasons 0 Eggs relatively resistant to chemical disinfectants 0 Can survive days to months in sewage and in moist shady soil 0 Risk factors hygiene ingestion of unwashed raw produce children playing in soil Echinococcus spp 9 can39t use Praziquantel Trichinella spiralis 2 distinct cycles A Urban or domestic T spiralis in pig rat human B Sylvan other species Distributionworldwide and most common in USA and Europe Disease trichinosis trichinellosis trichiniasis Smallest nematode to infect man World s largest intracellular parasite 0 Adults embed within cells of intestinal epithelium 0 Adults are intramulticellular Zoonotic disease 9 humans are dead end hosts Definitive and intermediate host are same infected animal As intermediate host 0 Adults within intestinal epithelium o NBL Jl within muscle cells Ovivaparous no eggs relased Primary reservoir host pigs Transmission eating raw or undercooked pork with newborn larva ll 0 From pork sausage in US Won t see NBL Jl in feces Life cycle 0 Humans can be both intermediate and definitive hosts 0 Adults in small intestine 0 Embed themselves into cells lining GI tract after mating o Rodent feces can contain Jl so can infect humans if the feces are eaten 2 Phases of Trichinosis Starts with eating NBL in park 1st phase enteral phase 0 Short term enteritis in small intestine o Gastroenteritis I Occurs a few days after infection I May mimic food poisoning I Parasite causes inflammation of epithelium of gut o Invasion and molting ofjuveniles to adults 0 Reinvasion and realease of NBL 5 days later 0 Host immunity expels adult parasites I Increased IgE with eosinophilia o 2quotd phase parenteral phase 0 Extraintestinal phase 0 Starts with migration and cell invasion by NBL o Fever muscle pain edema o No trophism for NBL invade all types of cells until they find striated muscle cells 0 Skeletal muscle cells are the only cells that survive invasion and support NBL growth I All other cells including cardiac striated muscle die 0 NBL predilection sites I 1st eye tongue masticulatory muscles I 2quotd diaphragm and intercostals I 3rd heavy muscles of extremities How Nurse Cell Complex forms in striated muscle cell 0 NBL with quot from 39 39 in I39 U o It induces morphological changes in invaded striated muscle cell 1 All contractile filaments lost I Myosin and actin 2 DNA replicates but arrests in GZ I Prevents production of new filaments I Enough gene expression to carry out metabolic pathways 3 Fibrous connective tissue capsule forms around cell 4 Circulatory rete formed around cell I Network of blood vessels capillaries 0 Completely changes muscle cell so it is no longer a muscle cell Vascular Endothelial Growth Factor VEGF o What stimulates angiogenesis o Produced by host cell under stimulation of parasite NBL o Stimulates host to form circulatory rete network of capillaries around nurse cell Trichinella spiralis NBL analogous to a virus o Parasite alters o Morphology of host cell 0 Gene expression of host cell 0 Functions of host cell 0 All changes benefit parasite only Parenteral Phase is Difficult to Diagnosis 0 Clinical signs aren t specific 0 Myositis muscle tenderness and edema myalgia o lfdiaphragm heavily infected may see dyspnea difficulty breathing o Bilateral edema around eyes Diagnosis and Treatment for Trichonosis o Dx muscle biopsy o If history of eating rawrare meat 0 Treatment analgesics for muscle pain Prevention 0 Don t eat rare or raw meat pork 0 Requires hard freezing o Hibernating animal freezing won t kill NBL in meat 0 Smoked does not mean cook Dioctophyme renale giant kidney worm 0 Giant 9 female is 100 cm long 0 Blood red in color 0 Definitive hosts large mammals fish eating carnivores and pigs horses cattle 0 Intermediate hosts annelid aquatic oligochete o Paratenic host fish frogs 0 Life cycle 0 13 penetrates stomach wall 0 Goes to right lobe of liver 0 Enters right kidney 0 Eggs out in urine Pathology 0 Destroys kidney o Dx eggs in urine 0 Patients with uremia severe hematuria 0 Treatment Albendazole and surgical removal Prevention 0 Don t eat undercookedraw fish 0 Don t drink untreatedunfiltered water Order Rhabditida 0 Common in soil STHs 0 Diversity of life cycles 0 Some alternate between free0living and parasitic cycles 0 Include Strongyloides stercoralis man primates dogs cats mammals and Strongyloides fuelleborni primates including man Rhabditiform larva o Juveniles are feeding and freeliving o Noninfective 0 Has rhabditiform esophagus 0 Has a bulb Filariform larva J3 o Nonfeeding o nfective for definitive host 0 Penetrate thru intact skin 0 Has filariform esophagus 0 Long and slender 0 Can t feed le is committed to be freeliving J3 has rhabditiform esophagus that is capable of surviving outside a host le is committed to being parasitic the J3 will have filariform esophagus that can t feed STRONGYLOIDES STERCORALIS quotthreadwormsquot 0 Distribution worldwide 0 Morphology very small worms 0 female 225 mm long 0 male 09 mm 0 Host niche small intestine o Transmmission Penetrate through skin by J3 2 Ingestion ofJ3 3 Autoinfection o le stays in gut long enough it can develop into J3 and penetrate intestine 4 Transmmary in pregnant women 0 Parasite goes to mammary gland and pass through milk to offspring 0 Source contaminated soil or water 0 Infective stage J3 filariform larva can swim HOMOGONIC LIFE CYCLE Only females are parasitic 0 Skin penetration 9 tissue migration heart and lungs9molt to J49 small intestine o Humans lungs in migration route 0 Tissue migration route varies lungs may or may not be part of route 0 Parasitic females parthenogenic o No males found 0 No sperm in parasitic females 0 Eggs of female embryonate without sperm n host 0 J3 skin penetration heart lungs o Molts in lungs914 up in bronchi swallowed o 9small intestine9molt to adults burrow anterior end into submucosa o 9eggs into gut lumen o 9eggs develop to J1 and hatch in gut ll out with feces n environment Pdevelop to freeliving males and females heterogonic cycle 0 911 9develop to infective J39infect new host parasitic cycle Autoinfection 0 ll retained in Gltract913 Penetrate gut mucosa Migrate up to SI Develop to adults Development of immunity keeps in check OOOO Hyperinfetion o Amplified infection via autoinfection o Immunocompromised individuals by steroids 0 Disseminate through body 0 Life threatening 0 Associated with high levels of steroids Normal immune response keeps in check steroids not indicated if suspect an individual infected with this parasite Steroids found to increase molting rate of parasite HETEROGONIC CYCLE quotfreeliving o Males and females 0 Mate 9 eggs in soil 0 Eggs hatch9Jl o 9 4 molts to produce free living adults OR o 9 2 molts to produce filariform J3 o Filariform larvae cannot feed and must find a suitable host or will die within 3 days Clinical Disease Penetration 0 Inflammatory response to 13s 0 Slight rash at entry site 0 Usually asymptomatic Pulmonary o Nonproductive cough wheezing eosinophilia in lungs 0 Only seen with large numbers of migrating juveniles 0 Lung damage by migratingjuveniles Intestinal requires heavy infection 0 Watery diarrhea with mucous and abdominal pain 0 Long term chronic colitismigrating adults damage tissues Autoinfection 0 ll retained in GI tract that develop into J3 o Penetrate gut mucosa o Migrate back to small intestine 0 Develop to adults 0 Development of immunity helps keep numbers in check 0 Hyperinfection causes this by using steroids 0 Amplified MASSIVE autoinfection for people given steroids 0 Steroids upregulate parasite molting rate molt faster I corticosteroids 0 Large numbers of parasites can disseminate through body 0 Potentially lethal Clinical Disease in S fuellebornie o SBS syndrome heavy infection 0 Distribution Papua New Guinea Africa 0 High morbidity and mortality in young children 0 Diarrhea malabsorption causes protein loss 0 Swollen belly syndrome 9 ascites from hypoproteinemia o Retarded physical and mental development 0 Effects reversible with anthelminthic therapy Strongyloides spp Transmission 0 Direct penetration by filariform 13 o Ingestion 13 in contaminated soil and water 0 Autoinfection o Transmammary Diagnosis 0 Juveniles in fecal smears o Autoinfection 0 Moderate infection numbers small 9 pool several samples 0 Must differentiate between S stercoralis and hookworm o ELISA for S stercoralis antibodies 0 Doesn t tell level of infection 0 Used to determine if someone needs steroids and could be infected o S fuelleborni 9 eggs in stool often in high numbers Treatment 0 verm ectin o TBZ thiabendazole 0 ALB albendazole o Reservoir hosts dogs primates 0 Infection associated with lack of sanitation feces in soil or water Hookworms Ancylostoma sp and Necator americanus o Morphology o Anterior curved end 0 Buccal cavity is armed for sucking host s blood 0 Muscular esophagus o Copulatory bursa in males 0 Distribution worldwide especially tropical and subtropical 0 Direct life cycle 0 Ingest J3 infective stage 0 Penetrate through intact skin 0 Hookworm infections result in 0 Iron deficiency o Anemia 0 Protein deficiency Host niche 0 Small intestine 0 Feed on blood and intestinal mucosal cells 0 Iron deficiency anemia from blood loss 0 Protein loss from blood consumption by parasite o Delayed mental and physical development in children Humans normal host for Ancylostoma duodenale and Necator americanus 0 These species differ in both pathogenicity and variations in life cycle Wrong host for A brazilienses and A caninum Patent patency when infection has progressed to point there is evidence of presence of parasite in host evident Pepatent not evident yet when parasite is going through development A duodenale teeth in buccal cavity 9 old world Ho Nu 0 Entry into host 0 Skin penetration o Transmammary o Transplacental o Ingestion of infected paratenic host oral ingestion ofJ3 is very rare for humans 0 Larger worm o Bigger blood sucker 0 28000 eggs per day 0 Hypobiosis in host up to 95 months 0 Remains dormant americanus cutting plates in buccal cavity most common in US 9 new world 0 Entry into host 0 Skin penetration only 0 Smaller worm o Smaller blood sucker 0 10000 eggs per day 0 No hypobiosis okworm Infection vs Disease 0 Infection asymptomatic o Invasion of body organisms that inhabit and reproduce in the body 0 Disease 9 infection producing clinical signs 0 Severity depends on 3 factors A Parasite load B Species of hookworm C Overall health of infected individual mber of Worms for Necator so drop down for A duodenale 0 Less than 25 asymptomatic 0 25100 mild disease 0 100500 moderate disease 0 Significant pathology 0 Iron deficiency anemia 5001000 severe disease o More than 1000 grave and potentially fatal Hookworm Clinical Disease 0 3 phases 0 Cutaneous phase dew itch ground itch I Local inflammatory response at penetration site Seen only in repeated infections Very pruritic itchy dermatitis Transient lesion not CLM 0 Pulmonary phase I To lungs 9 alveoli 39239 Asymptomatic 4 No melting in the lungs I Clinical signs require heavy infection 0 v Pneumonia symptoms 39239 Inflammation ofalveoli by 13 I 13 migrate up tracheal tree 9 swallowed o Intestinal phase I Most important with regard to pathogenesis I Symptoms depend on parasite load I Iron efficiency anemia o v Blood loss 39239 Abdominal pain 39239 lethargy I Anticoagulant prevents clotting 39239 Worm moves to new site old site keeps bleeding Poor nutrition hookworm disease 0 Protein iron deficiency anemia 0 Developmental retardation in children 0 Very heavy infections 9 death Infantile Ancyclostomiasis o Infected by 13 transmammary or transplacental 0 Develop severe anemia 0 Blood in stool melena black and tarry o Fail to thrive Diagnosis eggs in fecal smear 0 May see Jl must distinguish from S stercoralis 0 Can t differentiate hookworm species by eggs Treatment 0 Albendazole DOC o Mebendazole o Ivermectin 9 only partial efficacy for human hooks o Necator americanus has very low sensitivity 0 Improve nutrition if needed as well as drugs What about immunity to hookworms o Is not protective 0 Don t develop resistance to hookworms o Parasite load can build up over time What can happen if you get infected with 13 species of o Cutaneous larval migrans CLM or Plumber s itch o Aberrant hookworm infection human wrong host 0 Ancylostoma braziliensis dogs and cats and A caninum dogs 0 A braziliensis 0 Tropical and semi tropical regions including gulf coast of US 0 Treatment Thiabendazole topical ointment kills and shortens duration of condition and Albendazole Angiostrongylus cantonensis o Zoonosis rat definitive host man abnormal host 0 Distribution eastern hemisphere Caribbean and Louisiana 0 Indirect life cycle requires invertebrate intermediate host 0 Rat and snailslug 0 Causes CNS eosinophilic meningoencephalitis o 13 also shed in slime trails of snailsslugs 0 Life cycle o 13 eaten by definitive host 0 Obligatory migration to brain by 13 where it stops in human cycle 0 Clinical signs associated with CNS abnormalities 0 Severe headaches o In humans 0 Accidentally infesting snail or slug 0 Eating13 in slime trails on unwashed raw vegetablesfruit 0 Eating paratenic hosts rawundercooked Diagnosis difficult no specific tests Treatment 0 Mebendazole o Albendazole o Steroids if severe CNS signs Ascarids Round worms Greatest cause for parasitic infection by helmithes Ascaris lumbricoides roundworm 0 Distribution worldwide 0 Most common human helminthic infection 0 some regions of Africa 95 of population infected central and South America 45 US small pockets with problems 0 Host niche upper small intestine 0 Life cycle direct no vectors or intermediate hosts 0 nfective stage egg containing 13 stage 0 Ingest egg with 12 but conditions in SI stimulate molt to 13 immediately before it falls out of egg 0 Eggs very resistant 0 Thick shell I Impervious to anything that s not lipid soluble or a gas I Survive years in environment I Survive freezing o Require oxygen 9 embryonate 9 ll 912 o Won t hatch until it gets to the human GI tract I Gut provides required conditions I Allows molt of JZ 9 J3 I Activate egg enzymes for hatching I Prevents premature hatching and death of parasite in environment 0 Outer mucopolysaccharide coat very sticky 0 Life cycle 0 Egg with JZ ingested o JZ 9 J3 within egg in small intestine and then egg hatches o Obligatory tissue migration of J3 I Gut 9 liver 9 lung 9 gut Pathogenesis and Clinical Disease 0 Migratory phase asymptomatic if not heavy infection 0 Heavy infections I Lungs pneumonia molt to J4 I Molting substances are very antigenic I Eosinophilia and increased IgE levels induced 0 J3 can cross placenta I Continue development in fetus o Intestinal phase 0 No tissue pathology I Don t attach to gut I Parasites eat what you eat not you I Move against peristalsis to stay in place I Cuticle protects against digestive enzymes 0 Light infections are asymptomatic 0 Problems arise with heavy infections Heavy infections especially in children 0 Malabsorption o Stunting of gowth o Pot belly classic sign 0 Gut blockage 0 Causes crowding effect 9 adults will leave intestine 0 To stomach vomit worm or out thru nose 0 To gall bladder can cause obstruction 0 To ureters can destroy kidney 0 Penetrate gut wall cause peritonitis Diagnosis eggs in feces Treatment 0 Albendazole Mebendazole Ivermectin Pyrantel pamoate o Obstruction Piperazine 0 Not cidal o Paralyzes the worm 0 Expelled by peristalsis o Gut stasis immediate surgical intervention 0 Not gut sounds no movement within GI tract 0 Peritonitis is medical emergency 9 high mortality rate Prevention 0 Sanitary disposal of feces 0 Eggs from feces carried in dust carried by cockroaches and flies on feet 0 Eggs are sticky because of mucopolysaccharides 0 Stick to hands toys unwashed fruits and veggies 0 Stick on environmental surfaces including paper money 0 Highest prevlance where sanitation is low or nonexistent 0 Human feces as fertilizer Toxocara canis dog round worm o Smaller version o Prominent cervical alae 0 Typical ascarid eggs passed in feces 0 Same ascarid tissue migration 0 Gut 9 liver 9 lung 9 gut Visceral Larval Migrans 0 Because humans are wrong host 0 More serious than CLM o Ingestion of eg with 12 o 13 thru gut wall 9 bloodstream o Wanders in tissues 9 any organ 0 Wrong host wrong signals 0 Can t complete life cycle Organs most seriously affected CNS liver lungs eyes 0 Host response inflammation and formation of eosinophilic granulomas around 13 o 13 arrested development 9 don t grow anymore If eyes not involved 9 VLM If eyes involved 9 OLM Wuchereria bancrofti Brugia malaya o Microfilaria not 11 0 Advanced embryos o Infective stage for intermediate host mosquito 0 Don t cause the problems 0 Mosquito vectors 0 Culex aedes mansonia anopheles 0 Only a few speces in each genus o Humans primary source of parasite 0 Host niche lymphatics upperlower extremities genitalia Microfilaremia circulating levels of microfilaria in blood 0 Exhibits periodicity diagnostic but no clinical significance 0 Circulating from 10pm6am 9 Wuchereria bancrofti is nocturnal o Sequestered in lung capillaries at other times Pathogenesis of Lymphatic Filariasis 0 Results from host inflammatory and immune responses 0 No response to viable parasites o Parasites suppress host responses 0 Modulate it 9 THZ 0 Host response 9 dead and dying adult worms 0 What happens when worms die 0 Loss of immunosuppression Pathology 0 Lymphatic pathology occurs by 2 different pathways with same result 0 Responsive individuals caused by host immune response 0 Asymptomatic 9 direct action of parasite and its products 0 Secondary bacterial infections no known to play role in pathogenesis Wobachia sp mutualistic symbiotes 0 Produce endotoxinlike molecules 0 Damage vessels further 0 Enhance inflammatory responses in lymphatics 0 Don39t cause infection in humans Immunopathology o Narrowingoflymphatics o Infiltration of inflammatory cells 0 Hypertrophy of smooth muscle of vessels 0 Granuloma formation around worms 0 Dilation of lymph vessels enlarge 0 End result of dilated lymph vessels 9 occlusion of lymphatic vessels 0 Impede lymph flow lymphedema in affected area 0 Obstruction requires 2 things 0 Long time to develop 0 Repeated exposure to infection Symptom subjective abnormality experienced by patient that can t be quantified ex pain Sign objective abnormality indicative of disease that can be measure ex body temp Syndrome combination of signs and symptoms associated with a particular disease process Clinical Syndromes with Lymphatic Filariasis not a progression 0 Endemic normals o No clinical signs or microfilaremia day or night 0 Test positive with ELISA for circulating worm antigens 0 Evidence of mild lymphatic damage shown by imaging o Asymptomatic microfilaremics O O O O O No clinical signs Circulating microfilaria microfilaremia Diagnostic imaging shows direct damage by parasite I Lymphatic damage 39239 Dilated vessels and abnormal lymph flow I Kidney damage often 39239 Protein blood in urine Require treatment to stop internal damagae No transplacental transmission 9 fetus exposed to antigens 0 Acute filariasis O O 0 Acute lymphadenitis 9 lymphangitis I Swollen painful nodes I Inflammation of affected lymphatic vessels I Orchitis inflammation of testes Filarial fevers fever and chills Clinical signs caused by host responses to deaddying adult worms and worm associated antigens Recurring I Acute episodes flare up for about a week and subside I Episodes repeat in a few weeks I Debilitating to patient during flareups I Can go like this for monthsyears 0 Chronic obstructive disease ultimately leads to elephantiasis O 0 Severe lymphydema develops I Flow of lymph is impeded I Lymphatics are becoming obstructed Obstructive phase I Varicose lymphatics grossly dilated and tortuous I Chyluria back flow of lymph in urine I Hydrocoele lymphatic fluid accumulation in testes I Lymphedema in surrounding tissues 0 Can result in permanent condition called elephantiasis 0 Tropical pulmonary eosinophilia TPE 0 Not common 0 Mostly seen in young adult males in south India females can still get it o Asthmalike syndrome I Nocturnalcoughingwheezing I Eosinophils infiltrate in lungs o Hypersensitivity to microfilaria in lung capillaries 0 High levels of Ig E and circulating eosinophils gt70 0 Pulmonary lesion in lungs seen on xray 0 Can progress to chronic obstructive lung disease I Changes lesions to lungs becomes permanent and impede proper breathing Elephantiasis edema build up in tissues becomes firm and nonpitting requires years and repeated infections with adult worms 0 Fibrous connective tissue formation 9 scarring 0 Permanent blockage of lymphatics o No more edema permanent changes have occurred 0 Fibrosis and thickening of skin 0 Gross enlargement of involved tissues permanent and disfiguring Parasites are dyingdead and releasing the bacteria and their endotoxins 0 At site of daddying worms 0 Inflammatory infiltrate into vessel walls 0 Hypertrophy of smooth muscle in walls 0 Inflammatory infiltrate into vessel lumen to form granulomas around deaddying worms 0 All event serving to impede lymphatic flow Diagnosis for Filariasis o Microscopy 9 detection of circulating microfilaria stained blood smear o CFA circulating filarial antigens test 9 ELISA card test 0 Tests for worm antigens o Wuchereria bancrofti only 0 High sensitivity 0 100 specificity won t detect any others 0 Use for any time of day Treatment for Filariasis o 2 drug combo single dose yearly 0 DEC Albendazole 0 DEC Ivermectin o Albendazole Ivermectin 0 They are synergistic 9 combined action of 2 drugs together greater than each drug alone 0 All are 0 Safe 0 Inexpensive 0 Easy to administer 0 Effective with 1 dose Prevention and Control 0 Control of mosquito vectors is difficult o Sprays o Mosquito netting 0 Assume everyone in an infected area has it 9 all are treated 0 Daily use of DEC in fortified table salt Onchocerca volvulus onchocerciasis river blindness 0 Major cause of blindness in world from all causes 0 Distribution central Africa central and south America 0 No reservoir hosts 0 Host niche skin eye 0 Microfilaria migrate thru subcutaneous tissues 0 Adults in skin nodules o Micro laria are only ones that get into eyes 0 Microfilaria cause severe pathology include both dead and dying 0 Vector Simulium black fly 0 Live near rivers and streams I Requires water to produce 0 Long flight range several miles I Makes surrounding areas uninhabitable Clinical Disease 0 Onchodermatitis skin rash 9 due to dead and dying microfilaria o Rash o Intense itching pruritis I Host response to worm antigens 0 Can cause disfiguring skin changes sowda leopard skin I Depigmentation I Loss of elasticity I Wrinkling and cracking thickening o Onchocercoma formation nodule o Subcutaneous nodule that forms around adults 0 Fibrous connective tissue nodule surrounded by a network of blood vessels circulatory rete I Stimulation of host angiogenesis by parasite I Forms circulatory rete like Trichinella spiralis o 10 or more nodules is considered severe nodules o Ocular lesions 0 All parts of eye can be affected but cornea is major site 0 Sclerosing keratitis scarring and hardening of cornea major cause of blindness I Develops from chronic long term infections I Effects from host reponse to microfilaria in eye 0 Microfilaria in retina can also cause blindness o Inflammatory and immune response to microfilaria o Pathogenesis 0 Host response to dying adults microfilaria 0 Dead microfilaria induce intense inflammatory response 0 Lesions involve skin and eyes primarily How Parasite Evades Host Defenses o Pushes host immune responses to THZ type 0 Antibody is nonprotective o Suppress cell mediated immunity 0 Can actually interfere with skin test for TB tetanus and other vaccinations 0 When parasites die immunomodulation by parasite Diagnosis 0 Biopsy of nodule of skin skin snip if no nodule formation yet 0 Mazotti test NOT RECOMMENDED o Inject DEC into skin so it goes systemic o If microfilaria present they will be killed 0 Negative side 9 if individual is heavily infected could actually exacerbate the development of blindness by killing the microfilaria 0 Patch test variation of Mazotti test 0 Localized effect Treatment 0 vermectin 2 times a year 0 Add doxycycline to kill Wolbachia 0 Always excise nodule on head and neck because they re too close to the eye 0 Decrease possibility of microfilaria to the eyes Prevention and Control 0 Treated infected individuals with ivermectin 0 Vector control is iffy 9 insecticides sprayed over breeding habitat 0 Resistance has developed 0 Insects have long flight range


Buy Material

Are you sure you want to buy this material for

25 Karma

Buy Material

BOOM! Enjoy Your Free Notes!

We've added these Notes to your profile, click here to view them now.


You're already Subscribed!

Looks like you've already subscribed to StudySoup, you won't need to purchase another subscription to get this material. To access this material simply click 'View Full Document'

Why people love StudySoup

Jim McGreen Ohio University

"Knowing I can count on the Elite Notetaker in my class allows me to focus on what the professor is saying instead of just scribbling notes the whole time and falling behind."

Allison Fischer University of Alabama

"I signed up to be an Elite Notetaker with 2 of my sorority sisters this semester. We just posted our notes weekly and were each making over $600 per month. I LOVE StudySoup!"

Steve Martinelli UC Los Angeles

"There's no way I would have passed my Organic Chemistry class this semester without the notes and study guides I got from StudySoup."


"Their 'Elite Notetakers' are making over $1,200/month in sales by creating high quality content that helps their classmates in a time of need."

Become an Elite Notetaker and start selling your notes online!

Refund Policy


All subscriptions to StudySoup are paid in full at the time of subscribing. To change your credit card information or to cancel your subscription, go to "Edit Settings". All credit card information will be available there. If you should decide to cancel your subscription, it will continue to be valid until the next payment period, as all payments for the current period were made in advance. For special circumstances, please email


StudySoup has more than 1 million course-specific study resources to help students study smarter. If you’re having trouble finding what you’re looking for, our customer support team can help you find what you need! Feel free to contact them here:

Recurring Subscriptions: If you have canceled your recurring subscription on the day of renewal and have not downloaded any documents, you may request a refund by submitting an email to

Satisfaction Guarantee: If you’re not satisfied with your subscription, you can contact us for further help. Contact must be made within 3 business days of your subscription purchase and your refund request will be subject for review.

Please Note: Refunds can never be provided more than 30 days after the initial purchase date regardless of your activity on the site.