Parasitic Relationships



Protozoa – Intestinal and Urogenital

Entamoeba histolytica

Giardia lamblia

Cryptosporidium parvum

Cyclospora cayatenensis

Tissue and Lumen Protozoa

Trichomonas vaginalis

Pneumocystis carinii

Toxoplasma gondii

Blood Protozoa

Plasmodium

(P. vivax, P. falciparum, P. malariae

Leishmania

(L. donovani, L. tropica, L. mexicana, L. braziliensis

Trypanosoma

(T. cruzi, T. gambiense, T. rhodesiense

Bloodstream Nematodes (Roundworms)

Wuchereria bancrofti

Brugia malayi

Onchocerca volvulus

Loa loa

Dracunculiasis medinensis

Enteric Nematodes (Roundworms)

Strongyloides stercoralis

Ancylostoma duodenalis and Necator americanus

Ascaris lumbricoides

Enetrobius vermicularis

Bloodstream Trematode (Fluke)

Schistosoma

(S. mansoni S. japonicum, S. haematobium,

S. Dermatitis

Enteric Cestodes (Tapeworm)

Taenia saginata

Taenia solium

(Cysticercosis

Echinococcus granulosus

Parasitic Relationships

Parasites

Protozoa Metazoa

Sarcodina Nemathelminthes

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Sporozoa Platyhelminthes

•Sporozoans •Flatworms

Mastigophora

•Flagellates

Ciliates Trematoda Cestoda

•Ciliates •Flukes •Tapeworms

Definitions

Definitive Host: •Worms -Harbors Mature Parasite

•Protozoa –Harbors Sexually Reproducing Stage

Intermediate Host: •Worms -Harbors the Immature Parasite

•Protozoa – Harbors Asexually Reproducing Stage

Reservoir Host: Non-Human host that maintains the infection in nature

Vector: Transmits parasite from one host to next host

•Usually a Arthropod – Parasite undergoes obligatory lifecycle development

Transport Host: Direct transmission of parasite ie. fecal contamination by flies

•Intestinal Protozoa

|Parasite |Forms |Epidemiology |Transmission/ |Clinical Features |Diagnosis |Treatment |

| | | |Pathogenesis | | | |

|Entamoeba |Protozoa |•Worldwide distribution|•Fecal –Oral |Amoebiasis |Ova and Parasite Test |Drugs |

|Histolytica |•Cysts |•High risk associated |•Contaminated soil and water |•Mild diarrhea to fulminating dysentery |•Stool Samples are tested 3 |• Metronizadole + |

| |•8 Trophozoites |with poor sanitation |supplies w/ untreated feces |•Mucus, bloody diarrhea |sequential days |Diloxanide Furoate = 90% |

| |•extracellular | |•Direct contamination of food |•Fever, chills, tenesmus (anal sphincter |•Fecal sample is smeared on a |Cure Rate |

| | | |w/fingers,flies and cockroaches |spasm) and constipation |glass slide and stained |(Metronizadole – Lumenal |

| | | | |•Absesses in the intestinal tissue |•Microscopic examination |and Systemic |

| | | |Transmission Stage |•Dissemination – Sites of colonization |•Ova of worms |(Diloxanide Furoate - |

| | | |•Infection acquired by ingestion |-Lower right liver lobe (abcesses) |•Cysts/Trophozoites of |Lumenal |

| | | |of the CYST form |-2° Lung an brain ulcers |protozoa | |

| | | |•CYSTS are non-dividing, survives | | |Lumenal Drugs |

| | | |in water and dessication | |CYSTS – Spherical with 4 |Tetracycline, Paromomycin |

| | | |-Rigid cell walls | |nuclei |Diloxanide Furoate |

| | | | | |•Each nuclei: central dot |Systemic |

| | | |Disease Stage | |w/dense peripheral chromatin |Emetine |

| | | |•8 Trophozoites hatch from each | |TROPHOZOITES – divide by |Dehydroemetine |

| | | |cyst and colonize Large Intestine | |binary fission, disintegrate |Chloroquine |

| | | |•Phagocytic, ingest bacteria, | |in water | |

| | | |invades tissue, ingested RBC’s | |•May contain ingested RBC’s in|Prevention |

| | | | | |fecal samples |•Cysts are inactivated by |

| | | | | | |boiling, filtering and some|

| | | | | | |chemical agents |

|Giardia lamblia |•Trophozoite |Distribution is |Transmission |Giardiasis |•O & P Test |DRUGS |

| |are pearshaped |worldwide |•Ingestion of Cyst form |•Abdominal discomfort |•Trophozoites are fragile and |•Metronizadole |

| |( 8 external |•Hi Risk – Poor |-CYSTS are non-dividing, survives |•Foul smelling flatulence |difficult to ID even after |-Binds protein and DNA |

|Trophozoite |flagella, two |sanitation |in water and dessication |•Mild to Severe Diarrhea |staining |-inhibits RNA/DNA synthesis|

| |nuclei , parallel |•U.S. – epidemic and |-Rigid cell walls |•Some individuals – Intestinal |-The two nuclei look like two | |

| |axonemes |endemic more common | |maladsorption and/or lactose |eyes staring back at you | |

| |•Cysts are oval, |•Unfiltered surface |•Disease form – Trophozoite in |intolerance | |Prevention |

|• |four nuclei and |water in campers, |Small Intestine | |String Test - If Giardiasis is|•Cysts are inactivated by |

| |pair of axonemes |children at day care | | |still suspected, duodenal |boiling, filtering and some|

|• |•extracelluar |and male homosexuals | | |sampling for trophozoites is |chemical agents |

| | | | | |performed by swallowing | |

| | | | | |string, then pulling out | |

|Cryptosporidium parvum |Apicomplexan |•Humans |Transmission |Cryptosporidiosis |Diagnosis | |

| |protozoan |-Worldwide Distribution|•Fecal-Oral | | |•No effective drug therapy |

| |•intracelluar |•Cattle and Sheep |ie. Minneapolis -contamination of |1) Healthy Adults – Mild Diarrhea |•Oocysts in fecal smears |•No vaccine or means of |

| |•acid fast stain | |city water supplies by water run |2) Infants/Immunocompromised Adults |w/acid fast stain |prevention |

| | | |–off from manured fields following|•WATERY diarrhea, fever, dehydration and|•Serological Tests are NOT |−Filter and purify drinking|

| |•Oocysts – w/4 | |heavy rains |weight loss |available |water |

| |sporozoites | |•Infection by Oocysts (cysts) |•May result in death | | |

| |•Trophozoite – | |ingestion – w/4 sporozoites ea. |•AIDS – Bloody diarrhea, severe and | | |

| |Tissue sections | |•Sporozoites released in Sm. |chronic diarrhea | | |

| |resembles a | |Intestine⎝Infect columnar | | | |

| |trophozoite, but | |epithelial cells (sm/lg intestine)| | | |

| |is really a | |•Replicates in intracellular | | | |

| |“merozoite” | |membranous sac termed trophozoite | | | |

| | | |(actual merozoite) | | | |

| | | |-Asexual and Sexual cycles | | | |

| | | |-Sexual⎝Oocytes into feces | | | |

|Parasite |Forms |Epidemiology |Transmission/ |Clinical Features |Diagnosis |Treatment |

| | | |Pathogenesis | | | |

|Cyclospora cayatanensis |Apicomplexan |•Human – worldwide |•Fecal- Oral |• Diarrhea (up to 6 weeks) |•Cysts in fecal samples | |

| |parasite |distribution |•Contaminated Food | |-Round, Stain acid variable | |

| | |•Commonly found in | | |and fluoresces blue under UV | |

| |Cyanobacterium |travelers and | | |illumination | |

| |Like Body (CLB) |immunocompromised | | | | |

| | |adults | | | | |

| |•Cysts | | | | | |

|Enterocytozoon and Septata |Spores |•Humans – rare |•Fecal- Oral |Microsporidiosis |•Spore in feces or in Sm. | |

| |•Spiral polar |infections |•Spores -Spiral polar filaments |•Diarrhea |Bowel biopsy | |

| |filaments |-Found in intestinal |used to characterize |•Usually a complication of AIDS |•ID by spore polar filaments | |

| | |tract |− # coils in spore used for | |-# of spirals indicate | |

| | | |classification of generation | |generation | |

| | | |-Upon infection spiral filaments | | | |

| | | |protrude for penetration | | | |

•Tissue and Lumen Protozoa

|Parasite |Forms |Epidemiology |Transmission/ |Clinical Features |Diagnosis |Treatment |

| | | |Pathogenesis | | | |

|Trichomonas vaginalis |Unicellular , |Humans |SEXUAL INTERCOURSE |Vaginitis |•Saline Smear |Metronidazole |

| |Flagellated |•Urogenital tract of |•Trophozoite transmitted |•Most common cause of vaginitis worldwide|•View under microscope |-mixed a amebicide |

| |Eukaryote |humans |•Cannot survive outside of host |•Women - >>50% symptomatic | |-Inhibit DNA/RNA synthesis |

| |•Facultative |-Vagina and urethra for|•Extracellular Parasite damages |-Foul smelling, greenish discharge | |-Disulfiram like rxn with |

| |anaerobe |women |epithelial layer in urogenital |-Burning , itching | |ethanol |

| | |-Seminal Vesicle, |tract |•Men – Most asymptomatic | |-SE: GI, metallic taste, |

| |Motile Trophozoite|prostate and urethra | | | |CNS –dizzy, numb, |

| |•4 anteriior |for men |Pathogenesis | | |neuropathy, neurotoxicity |

| |flagella w/5th |•No intermediate |•Contact dependent cytoxicity | | | |

| |recurrent |reservoir hosts or |•Inflammation of epithelium | | | |

| |flagellum imbedded|sexual stages | | | |**Need to treat both |

| |in membrane |•25-50% women in US |Hydrogenosome Organelle | | |sex partners** |

| |•NO CYST |have organism |•Proteins needed for cytoxicity | | | |

|Pneumocystis carinii |Extracellular |•Normal commensal |Transmission |Pneumonia |•Sputum specimen |HIV |

| |Fungi |•Causes problems w/very|•Airborne |•Lung pathology |•Bronchial brushing or |•CD4 count >>50% of | | | | |

| | |AIDS cases | | | | |

|Toxoplasma gondii |Intracellular |Intermediate Hosts |Transmission |Toxoplasmosis |Acute and Congenital Diagnosis|DRUGS |

| |Apicomplexa |•Humans and other |•Contact w/feline feces |•Immunocompetent – asymptomatic |•Immunofluorescence assay for |•Pyrimethamine |

| |Parasite |mammals |•Ingestion of infected undercooked|•Primary infections in immunosuppressed |IgM Ab |-Drug of choice |

| | |Definitive Hosts |meat |resembling Mononucleosis, disseminated |Acute |-Antifolate drug |

| |•Oocytes -cat |•Cats – Sexual |•Transplacental Transmission to |disease or encephalitis |•Microscopic stained preps |•Sulfadiazine + |

| |feces |gametocytes fuse to |human fetus – Only during |•Congenital infection –abortion, |show crescent shapeed |Pyrimethamine |

| |•Pseudocyst in |form oocysts ⎝feces |pregnancy |stillbirth, neonatal disease , seizures, |trophozoites | |

| |meat | |Pathogenesis |w/encephalitis, chorioretinitis, |•Cysts may be seen in tissue |Prevention |

| |•Tachyzoite | |•Specialized structures at end of |hepatosplenomegaly, fever, jaundice and |•Cell culture and innoculation|•Cook meat thoroughly |

| |(liver) | |cell for receptor-mediated |intracranial calcifications |into mice |•Pregnant women avoid |

| |•Pseudocyst | |invasion ⎝inside cell organism |-Many newborns may be asymptomatic | |undercooked meat and cats! |

| |w/Bradyzoites | |w/in phagosome |w/manifestations years later | | |

| | | |•Inhibition of lysozome with | | | |

| | | |phagosome | | | |

| | | | | | | |

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•Blood and Tissue Protozoa

|Parasite |Forms |Epidemiology |Pathogenesis |Clinical Features |Diagnosis |Treatment |

|Plasmodium |Apicomplexa |Geographic |•Mosquito Vector – Saliva |Malaria (incub 1-3wks) |Hemozin –Insoluble product of |Antimalarial Drugs |

| |Intracellular |•Africa, Asia, India, |Asexual Lifecycle |•hemolytic anemia, splenomegaly, |Hb degradation (heme) |•Primaquine (oral) |

|P. vivax |Parasite |South/Central America |•Sporozoites in Mosquito |hepatomegaly, renal damage, GI and |•You can diagnose w/ presence |-Tissue schizonticide |

|P. falciparum | |•2nd most deadly single|bite⎝Human Liver |superinfection |of malarial pigment – in |-Gametocidal (all 4) |

|P. ovale | |human-infectious agent |(hepatocytes)-multiply to form |•Synchronization of RBC rupture by mature|parasitized cells |-Cures only P. vivax and |

|P. malariae |•Sporozoite | |Merozoites⎝ rupture hepatocytes |schizonts | |ovale |

| |•Merozoite |P. vivax and P. |and invade RBC’s⎝Becomes |•Temp. reset to 41°C, Chills, then |•Blood Smear and stain |-Hemolytic anemia |

| |•Schizont |falciparum account for |Trophozoite feeds on RBC |Fever, Fever breaks, Sweat glands open |•Signet ring shaped |•Chloroquine |

| |•Trophozoite |>>>95% of all cases |contents⎝Becomes a Schizont (16-32|and drenching sweat follows |trophozoites |-Blood schizonticide |

| |•Gametocyte |P. malariae ~4% |nuclei w/in RBC)⎝Ea. Nucleus |•Cycle repeats in regular periodicity |•P. falciparum gametocytes are|•Quinine |

| |•Zygotes |P. ovale – very rare! |w/cytoplasm pinches off to form |-P. vivax (48hr) Benign tertian malaria |crescent shaped |-Blood schizonticide |

| |•Oocyte | |new Merozoite |-P. falciparum (48hr ) Malignant |•Others are spherical |•Pyrimethamine |

| | |P.vivax –temperate |⎝RBC ruptures w/new RBC |tertian malaria | |•Chloroguanide |

| | |zones, tropics and |infected ⎝Repeat cycle |-P. ovale (72hr )Benign quartan malaria | |•Mefloquine |

| | |subtropics | | | |-Blood schizonticide |

| | |P.falciparum-tropics | |P. falciparum – Most pathogenic •Most | |-Unknown mechanism |

| | |and subtropics |Sexual Lifecycle |deaths esp non-immune individual ~50% | |-membrane damage |

| | |•Most severe and life |Some Trophozoites in RBC become |mortality | |-P. faliparum is resistant |

| | |threatening |micro/macrogametocytes |•Differences include: Infects all RBC’s, | |-CNS effects |

| | |•Children and elderly |⎝release in blood w/rupture of |(level of parasitemia, ( merozoite | | |

| | |at risk |RBC⎝Tranfer to feeding |asexual reproduction, (RBC destruction | |*Many are drug resistant |

| | | |mosquito⎝Fertilization of |(⎢O2 for tissues), RBC membrane b/c | | |

| | |Epidemiology |gametes⎝Zygotes ⎝Oocytes⎝ |sticky (knobs) and adhere to endothelial | |No vaccine! |

| | |•Blacks more |1000’s Sporozoites⎝Mosquito |wall ⎝plugged capillaries and vessels | | |

| | |susceptible than whites|Salivary Glands⎝Bite Host |(cerebral malaria) | | |

| | |•Sickle cell provides | | | | |

| | |protection | |P. falciparum and P. ovale | | |

| | | | |•Chronic –symptoms often disappear | | |

| | | | |Recrudescence – Controllable # parasites | | |

| | | | |remain in bloodstream and reactivate | | |

| | | | |w/trauma/immunosuppressed | | |

| | | | |Relapse –Sporozoites dormant | | |

| | | | |(hypnozoites) in liver and reactivate | | |

|Leishmania |Intracellular |Reservoir Hosts |Transmission |Leishmaniasis (incub wks to months) |Diagnosis |Visceral Disease |

| |Kinetoplastid |•Rodents and Dogs |•Bite of the Sandfly saliva |•Lesions Bite Site –Tissue damage due to | |•Sodium Stibogluconate |

|L. braziliensis |Protozoa | |•Promastigotes ⎝bloodstream⎝ |lytic products of dying Mφ’s |Visceral Disease |-IV |

|L. mexicana |•Amastigote |L. braziliensis |Amastigotes infect Mφ’s |Cutaneous Disease –Ulcerated Lesions – |L. donovoni |-inhibition of parasite |

|L. tropica |•Promastigote |•mucocutaneous/ |(ingested)-attachment with |Raised edges, wet/dry crusty center w/ |•Amastigotes in BM, Spleen, |glycolysis (exact mech. |

|L. donovani |•Epimastigote |cutaneous |LipoPhosphoGlycan (LPG) |spontaneous healing in 6-12 months |Lymph node biopsy |unknown) |

| |•Trypomastigote |•New World |Glycoprotein 63kDa (gp63), |•CMI response and immunity |specimens |-Eliminated by urine |

| | |L. mexicana |complement receptor on |Mucocutaneous Disease – mon-yrs later |•Smears or Culturing of WBC’s | |

| | |•cutaneous |Mφ⎝Amastigotes survive @pH4 |destruction of mid-face |or BM |No vaccine |

| | |•New World | |•Death w/starvation or aspiration | | |

| | |L. tropica |•Hi risk to military, travellers, |Visceral Disease (Kala Azar)– Amastigotes|Mucocutaneous/Cutaneous | |

| | |•cutaneous |AIDS pts. |replicate in cells of reticuloendothelial|•Amastigotes in skin lesions | |

| | |•Old World | |system ⎝Liver, Spleen, BM w/incub | | |

| | |L. donovani | |wks-yrs | | |

| | |•Visceral | |-Diurnal fever, hepatosplenomegaly, | | |

| | |•Old World | |immunosuppression, wt. Loss, diarrhea, | | |

| | | | |cough, nose bleeds, lymphadenopathy | | |

|Parasite |Forms |Epidemiology |Transmission/ |Clinical Features |Diagnosis |Treatment |

| | | |Pathogenesis | | | |

|Trypanosma | |T. gambiense – •Humans |•Tsetse Fly Bite |Trypanosomiasis –African Sleeping |•Blood smear |Melarsoprol (IV) |

| |•Trypomastigotes |ONLY |•Short Stumpy trypomastigotes |Sickness |•Culture of blood, lymph or |-CNS SE |

|T. gambiense |•Procyclic Stage |•W.Africa |(nondividing) ingested during |•Chancre at site of bite, weekly fever, |CSF |-Short t ½ |

|T. rhodesiense |•Metacyclic Stage |•Death – Months/Yrs |blood meal of Tsetse Fly⎝Midgut |lymphadenopathy | |-Hemolytic anemia |

| | |T. rhodesiense |-Procyclic Stage⎝Metacyclic |•Myocarditis, Gamma-Globulinemia and | |-SE: hypersensitivity, |

| | |•Wild animals |trypomastigotes in salivary |generalized immunosuppression | |abdominal pain, vomit |

| | |(zoonosis) |glands⎝Bite ⎝Local multiplication |Chronic Infection | |-meningoencephalitis Rx for|

| | |•E. Africa |at bite site⎝ |•Invasion of CNS-lethargy, personality | |T. gambiense and T. brucei |

| | |•Death – Wks/Months |inflammation |changes and insomnia | | |

| | | | |•Coma due to demyelinating encephalitis | |Suramin |

| | | |•Dissemination through bloodstream|⎝headache, insomnia, mood changes, ms | |-prophylactic |

| | | |and lymphatic system |tremors, slurred speech, apathy then | |-inhibits enzymes⎝ inhibits|

| | | |⎝parasitemia and antigenic |somnolence, coma | |nrg metabolism |

| | | |variation |•Untreated disease is fatal ⎝ pneumonia | |-SE: GI, shock, |

| | | | | | |unconscious, urticaria, |

| | | | |Antigenic Variation | |neurological |

| | | | |•Allows parasite to evade humoral | | |

| | | | |response | |Pentamidine |

| | | | |•Variant Surface Glycoprotein -VSG | |-T. gambiense nematologic |

| | | | |-10% of parasite protein w/>100genes | |stage only |

| | | | |for Antigenically Different Genes | | |

| | | | |•Cyclic fever as result of Ag variation | | |

|T. brucei | |•Infects Cattle | | | | |

| | |•Does Not infect Humans| | | | |

|Trypanosma cruzi | |Habitat |•Reduviid Bug (Kissing Bug) |CHAGA’s Disease – American |Acute Disease |Nifurtimax |

| | |•Humans and animals |-Parasite in natural cycle |Trypanosomiasis |•Trypomastigotes in Blood |-ONLY suppresses does NOT |

| |•Trypomastigotes |•South and Central |-Transmitted when feces wiped into|Acute Disease |Smears |CURE acute Chaga’s disease |

| |•Intracellular |America |abraded skin or puncture |•May last up to 2 months |•Amastigotes in muscle cells |-SE: CNS, hypersensitivity,|

| |amastigote |•Wild animals in U.S. |wound/mucous membranes (eye) |•Fever, malaise, lymphadenopathy, |or BM |GI |

| | |-No vectors for human |-Local replication in Mφ and |splenomegaly, hepatomegaly and |-Bone marrow biopsy or muscle | |

| | |infection |consquent infiltration of cells |myocarditis |biopsy | |

| | | |and fluid ⎝swelling (chagoma) |•Amastigotes nests in muscle cells | | |

| | |Infection – Most common| |Intermediate Stage |Chronic Disease | |

| | |in children |•Also transmitted by ingestion, |•No evidence of parasite in blood or |•Serologically | |

| | |under 10yrs old |blood transfusions and organ |disease |•Xenodiagnosis | |

| | | |transplants |Chronic Stage | | |

| | | | |•Years to decades later | | |

| | | |Pathogenesis |•Cardiomyopathy, Cardiac Arrythmia, CHF, | | |

| | | |•Amastigotes can kill cells and |Megasyndrome (heart, colon, esophagus), | | |

| | | |cause inflammation w/mononuclear |Meningoencephalitis in AIDS pts. | | |

| | | |cells | | | |

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•Bloodstream Nematodes - Roundworms

|Parasite |Forms |Epidemiology |Transmission/ |Clinical Features |Diagnosis |Treatment |

| | | |Pathogenesis | | | |

|Wuchereria bancrofti |•Microfilaria |•Humans are Definitive |•Female Mosquito Bite |FILARIASIS |Diagnosis |• Diethylcarbamizine |

| |-Sheathed |Hosts |•Mosquito acquires microfilaria |•Spectrum of Disease dependent on worm |•Problem is nocturnal |-Rapid GI absorption |

| |-L1 Larva |•Occurs in humid tropic|stage L1 larva fr. Bloodmeal |burden with pathology due to Death of |periodicity |-⎢muscle activity and |

| |-L2 Larva |areas with mosquito |⎝Mosquito muscle L2 Larva |ADULT worms |•Provocative Challenge |paralyzes leaving |

| |-L3 Larva |distribution |⎝Salivary Gland L3 Larva |•Asymptomatic w/low level infection |Microfilaria can be induced to|susceptible to host defense|

| |•Adult Form |•200-300million people |⎝Human via bite |Ηigher levels of infection |migrate from deeper blood |-partial metab. ⎝elimin. in|

| | |are infected | |•Filarial Fevers, Tropical Pulmonary |vessels to peripheral |urine |

| | | |Characteristics |Eosinophilia & Blocked Lymphatics |bloodstream with |-SE due to dying worms: GI,|

| | | |•Adult worms live in lymph nodes |•Fibrosis and calcification around dead |diethylcarbamizine |lymphadenopathy, joint |

| | | |for 5-8 years |adult⎝Lymphadenitis⎝Lymphangitis (2° | |pain, fever, chororetinitis|

| | | |•Females give rise to live |infection) distal to node w/trapped adult| | |

| | | |microfilaria larva (live 1-2yrs) |•Acute Fever, Local Edema,Back/Head | |Ivermectin |

| | | |-Appear in bloodstream with |Aches, Lymph Hydrocele | |•Being tested successfully |

| | | |Nocturnal Periodicity (peak |Chyluria- Rupture of Lymph Gland | | |

| | | |10pm-2am) |Hydrocele releasing fluids into urine | | |

| | | |-Coincides w/mosquito feed time |Elephantiasis-Legs, Arm, Scrotum, Breasts| | |

| | | | |(HUGE!) | | |

| | | |Wuchereria – microfilaria are | | | |

| | | |sheathed w/ NO nuclei in tail | | | |

|Brugia malayi |•Same as above |•Same as above |•Same as above except: |•Same as above |•Same as above |•Same as above |

| | | |-microfilaria are sheathed with | | | |

| | | |2 nuclei in tail | | | |

|Onchocerca volvulus |•Microfilaria |Habitat |•Black Fly Bite |Onchocerciasis-River Blindness |Diagnosis |Suramin |

| |-Unsheathed |•Central Africa – fast |•Adults live as pairs in |•Nodules –Over bony areas such as the |•Microscopic observation in |•Drug of choice |

| |•Adult Form |rivers |subcutaneous nodules (10-15yrs) |head, spine, pelvis and knees |skin snips (migration out onto|•SEVERE SE: GI, Shock, |

| | |•Central America-slow |•6-12months after infection⎝ |•C. America – Upper body |saline) |Unconsciousness, |

| | |rivers |Female gives rise to live |•C. Africa – Lower body (flight height) | |neurological, urticaria |

| | | |microfilaria | | | |

| | | | |Disease- Cellular immune response to the | |Ivermectin –sterilizes |

| | | |Microfilaria (nonsheathed) |DEATH of the Microfilaria | |females for ~6months |

| | | |•Spend 1-2 yrs migrating thru |•Βlindness - Lesions in cornea, iris, | | |

| | | |subcutaneous tissue including the |retina causes iritis and corneal | |*Diethylcarbamizine |

| | | |EYES |keratitis | |increases pathology of |

| | | | |•Onchocercal Dermatitis– Death in subQ | |disease |

| | | | |tissue ⎝itching, rashes, pigmentation | | |

| | | | |(’s⎝edema, fibrosis, thickening of skin | | |

| | | | |and loss of elasticity | | |

|Loa loa |•Microfilaria |Central W. Africa |•Mango/Deer Fly Bite |Loiasis-African Eye Worm |Diagnosis |•Diethylcarbamazine |

| |-Sheathed | |•Adults migrate thru SubQ and Deep|•Itching/Inflammatory Response in |•Blood Smear visualization |eliminates microfilaria |

| |•Adult Form | |tissue |travelled route of migration | |•Surgically removed during |

| |3-7cm | | | | |passage to eye |

| | | | |Calabar Swellings (Lasts 2-3 days) | | |

| | | | |•Bumping of limb illicits release of | | |

| | | | |irritants from worm (hypersensitivity | | |

| | | | |reaction) | | |

| | | | |•Migration over nose is painful | | |

|Dracunculiasis medinensis |•L1 Larvae |•Humans |•Infected copepod⎝ingested in |Dracunculiases-Guinea Worm |•Head of worm in the skin |•Adult is wound out on a |

| |•L3 Larvae |•Copepod is vector |unfiltered water then migrates |•Painful Nodules – Adult lives in; lower |ulcer |stick 2cm/day |

| |•Adult |•Africa, India, |-Ruptured nodule contaminates |extremities of leg | |Prevention –Boiled filtered|

| |60-100cm |Pakistan |water ⎝copepod ingests ⎝L3 |•Nodule erupts⎝L1 into environment | |drinking water |

•Enteric Nematodes – Roundworms

|Parasite |Forms |Epidemiology |Transmission/ |Clinical Features |Diagnosis |Treatment |

| | | |Pathogenesis | | | |

|Strongyloides stercoralis |•Adult females |Habitat |Transmission |Strongyloidiasis |Diagnosis |Thiabendazole |

| |2-3mm |Female worms are |•Direct contact with soil |•Skin penetration – unnoticed w/low worm |•See Larvae in Fecal Wet |•Used to treat very ill |

| |•Adult male |embedded in mucosa of |containing infective larvae |burden or local erythema/pruritis |Mounts |side effects |

| |•Larvae |duodenum and jejunum |•Larvae penetrate unbroken skin |•Epigastric Pain |•See Larvae in formalin-ethyl |•microtubule inhibitor and |

| |Filarial |•Worldwide |Direct Cycle |•Diarrhea |acetate fecal concentrates |⎢ glucose uptake |

| |-infective |•Warm, humid |Infective larva in soil⎝Larva |•Urticarial rash (hives) common in | |•( toxicity |

| |Rhabditiform-non-i|environments w/poor |penetrates skin⎝Larva carried to |chronic infection |Serology |•Nausea, dizzy, vomit, |

| |nfective |sanitation and soil is |lung via blood⎝developing larva in|•Loeffler’s Syndrome |•Elisa will detect Ab, but |anorexia |

| | |contamninated w/human |sputum⎝Adult worm in GI |(Coughing, wheezing and transient |cannot distinguish present or |•allergic hepatitis if |

| | |feces,fecal material |(swallowed) ⎝Noninfective larva in|pulmonary infiltrates |past infection |>2days |

| | |for fertilizer |feces |(Eosinophilia | | |

| | |•approx. 100million |Non-Direct Cycle | | |•2day course |

| | |infected |Non-infective larva in soil⎝Free |Hyperinfection –Large numbers of larvae | | |

| | | |living adult in soil⎝eggs in |transform into infective stages⎝ | | |

| | | |soil⎝non-infective⎝infective larva|Invade intestine and/or lungs | | |

| | | |in soil⎝Penetrate |-Severe, bloody diarrhea | | |

| | | |skin⎝Lung⎝Sputum⎝GI⎝ |-Cough, dyspnea, wheezing and hemoptysis | | |

| | | |Non-infective larva in feces |Disseminated Strongyloidiasis | | |

| | | |⎝Repeat of cycle |Migrating larvae in other organs: Liver, | | |

| | | |Autoinfection – Larva in intestine|Heart, Kidneys or CNS | | |

| | | |may develop into infective larva, |•Usually in malnourished or | | |

| | | |penetrate mucosa⎝lungs for another|immunosuppressed (AIDS) pts | | |

| | | |cycle of development |•Hi doses of corticosteroids ppt | | |

| | | | |dissemination | | |

|Angylostoma duodenale |•Adult 1cm |Habitat |Transmission |Hookworm Infection |Diagnosis |Mebendazole |

| |•Embryo |•Adult worms attach to |•Direct contact w/soil containing |•Erythematous and Pruritic Lesion at |•O&P 3X |•Microtubule disassembly |

|Necator americanus |•1st stage larva |mucosa of duodenum and |infective larvae |penetration site |•Examine Fecal Specimens | |

| |•Infective larva |proximal small |A. duodenale – Infection via |•Loeffler’s Syndrome |by concentration techniques |Pyrantel Pamoate |

|(Hookworm) |•Life span of |intestine |ingestion of larva w/buccal |-Transient pulmonary infiltrates and |-Larvae may hatch in fecal |•Depolarization of neurons |

| |adult is 1-5yrs |•Warm and Moist climate|cavities that have cutting plates |eosinophilia during lung migration |specimens that are not fresh |⎝blockade |

| | |•Regions w/poor |N. americanis – buccal cavities | |therefore 3X |•Paralysis and expulsion |

| |Adult Parasite |sanitation |have pairs of teeth |Symptoms | |from intestine |

| |•Anterior end is |•Rural areas up to 90% | |•Proportional to Worm Burden | | |

| |hooked |infection rate |Life Cycle– Eggs passed in |•Light infections – GI asymptomatic | | |

| |•Specialized |•∼1/4 of world |stool⎝Develop into 1st larvae and |•Moderate –Epigastric Pain, Diarrhea | | |

| |buccal capsules |population infected |hatches w/in 48hrs⎝Feed on organic|and mild Eosinophilia | | |

| |for sucking on | |material in soil⎝Non-infective |•Anemia – secondary to blood loss will | | |

| |intestine mucosa | |larva⎝Infective larva⎝Penetrates |depend on the numbers of worms, dietary | | |

| |•Males have | |skin⎝Lung by blood⎝Developing |iron intake and iron stores in pt | | |

| |copulatory bursa | |larva in sputum ⎝Swallowed into GI| | | |

| |at posterior end | |⎝Eggs in feces | | | |

| | | |Intestine –Attaches to mucosa and | | | |

| | | |sucks blood, mate in lumen and | | | |

| | | |female lays eggs | | | |

|Parasite |Forms |Epidemiology |Transmission/ |Clinical Features |Diagnosis |Treatment |

| | | |Pathogenesis | | | |

|Ascaris lumbricoides |•Adults Form |Habitat |Transmission |Ascariasis |Diagnosis |Mebendazole, Pyrantel |

| |20-35cm |•Lumen of Small |•Ingestion of embryonated eggs |Lung Phase |•Microscopic detection of eggs| |

|(Giant Round Worm) |-Largest |Intestine |from fecally contaminated food or |•Larval migration in lung is usually |in stools | |

| |intestinal |•Worldwide |beverages, fomites or dirty |asymptomatic except in heavy infections |-Eggs are brownish in color | |

| |nematodes |•Poor sanitation |fingers |or in sensitized individuals |and bumpy outer coat | |

| |-Lives up to 1yr |•Highest rates in areas| |•Pneumonia |-infectious after 2-3wks of | |

| |-Look like large |w/human excreta used |Life Cycle |•Loeffler’s Syndrome |larval development in | |

|Male |earthworms |for crop fertilization |Embryonated egg in soil⎝Egg |Intestinal Phase |egg-shell | |

|Female |•Larva |•Up to 1 billion |ingested⎝Larva hatches and |•Abdominal Pain |•Worms in feces | |

| | |infections |penetrates intestine⎝Larva carried|•Diarrhea | | |

| | | |to lung⎝Developing larva in sputum|•Non-specific GI complaints | | |

| | | |and swallowed⎝Adult worm develops |•Intestinal obstruction –esp. heavy | | |

| | | |in intestine⎝ |infections in children | | |

| | | |Eggs in feces |•Invasion of Bile Ducts-Liver abscesses, | | |

| | | | |cholangitis, bile duct obstruction, | | |

| | | |•Female adult deposits >200K eggs |pancreatitis | | |

| | | |per day |•Worms may be vomited or actively migrate| | |

| | | | |up esophagus and out of nasopharynx | | |

| | | | |•Mild-Moderate EOSINOPHILIA is common | | |

|Enterobius vermicularis |•Adult |Habitat |Transmission |Enterobiasis |Diagnosis |Treatment |

| |-Female 1cm |•Adult Worms live in |•Ingestion of eggs from |•Majority asymptomatic |•SCOTCH TAPE applied to anal |Mebendazole and Pyrantel |

|(Pinworm) |and have a sharp |colon, cecum and |environment |•Anal pruritus |folds and perianal skin in |Pamoate in single dose |

| |pointed posterior |appendix |•Autoinfection -Fecal-Oral route |•Vagina pruritis (due to migration) |morning b/f going to bathroom | |

| |end like a pin |•Worldwide w/high |via fingers, etc. |•NO evidence of causing appendicitis |or bathes | |

| | |prevalence in school |•Inhalation of eggs that adhere | |•Microscopic examination of | |

| | |children (20-40%) |to mucus membranes and swallowed | |tape for pinworm eggs | |

| | |•Most common helminthic| | |•3-4X will diagnosis infection| |

| | |infection in U.S. |Life Cycle | | | |

| | | |Embryonated egg in environment or | |•7X consecutive (-) swabs to | |

| | | |on fingers⎝Egg ingested⎝ egg | |exclude | |

| | | |hatches in intestine⎝Adult worm in| | | |

| | | |intestine⎝Gravid female migrates | | | |

| | | |to anus⎝Eggs deposited on perianal| | | |

| | | |skin | | | |

|Trichuris | |Habitat |Transmission |Mostly asymptomatic |O&P |Mebendazole |

|trichiura | |•Soil |•Ingestion of Eggs in soil |•Diarrhea | | |

| | |•Human intestine |•Intestine⎝Immature adults migrate| | | |

|(Whipworm) | |(colon) |to colon⎝mate⎝1000’s | | | |

| | |•Worldwide |eggs/day⎝feces | | | |

| | | | | | | |

| | | | | | | |

| | | | | | | |

| | | | | | | |

•Trematodes -Flukes

|Parasite |Forms |Epidemiology |Transmission/ |Clinical Features |Diagnosis |Treatment |

| | | |Pathogenesis | | | |

|Trematodes and |Adaptations by Trematodes and Cestodes |

|Cestodes |1) Adhesive organs for attachment to host ⎝Anterior suckers or hooks |

| |2) Modifications for obtaining nutrients⎝Absorbance thru body wall, specialized ingestion and storage organs |

| |3) Increased reproductive capabilities |

| |4) Evolved larval stages for passage from host to host |

|Schistoma mansoni |•Cercaria Larva |Habitat |Transmission |SCHISTOSOMIASIS |Diagnosis |Praziquantel |

| |-human infective |•Affects GI Tract |•Fresh water cercaria larva bores |•Itching and dermatitis followed by |•Eggs in stool, Blood in stool|•( Calcium permeability and|

| |form | |under skin |fever, chills, diarrhea, lymphadenopathy |or Rectal biopsy |( Ab adherence for |

|(Trematode) |•Schistosomula |Definitive Hosts | |•Granulomas in liver due to eggs | |leukocyte attack |

| |-human migratory |•Humans |Life Cycle |⎝fibrosis, hepatomegaly, portal | |•Rapid absorption in CSF |

| |form |•Endemic areas patients|Cercaria Larva hatches fr. Snails |hypertension (splenomegaly) | |•Short t ½ - liver |

| |•Adult |2-30yrs old |⎝Bores under skin⎝ |-Due to Antigens secreted by eggs | |•CNS SE: dizzy, anorexic, |

| |-Liver |•Infection rare in |Schistosomula⎝Migrate to |-Hepatocytes are usually undamaged ⎝Liver| |malaise, GI |

| |-Live 5-30yrs |middle or old age |lymphatics and blood vessels⎝ |function tests remain normal | | |

| |•Eggs | |Liver dev. Adult Worms (100-1000 |•Intense Eosinophilia | | |

| |•Miracidium Larva |Intermediate Hosts |eggs/day)⎝Portal Veins, |•Chronic Salmonella Infection | | |

| |-Ciliated Snail |•Aquatic Snails |Superior/Inferior Mesen-teric |•Acute hepatitis, Cirrhosis | | |

| |infective form |•Africa, Middle East, |veins⎝Mate⎝Eggs work out of |•Calcified bladder | | |

| | |Carribean, South |veins⎝Bladder, Intestines ⎝Eggs |•Bladder carcinoma | | |

| | |America |passed in urine/feces⎝ Fresh water|•Neurological Problems (parasites or | | |

| | |•~200 million people |Environment devel. Miracidium |eggs in CNS) | | |

| | |infected |larva⎝Infects Snail⎝Cercaria Larva| | | |

| | |•2nd to malaria for |and released |Liver Stages | | |

| | |infectious deaths | |Hepatosplenomegaly, eosinophilia, and in | | |

| | |•~200K deaths/yr |Pathogenesis |severe cs ⎝abdomen becomes filled w/fluid| | |

| | | |•Due to presence of EGGS in Liver,|and hepatosplenomegaly | | |

| | | |Spleen, or Gut/Bladder Wall |Immune Response | | |

| | | | |•Ab dependent; CD4 Tcells | | |

| | | | |•IgE Mφ, IgE/IgG eosinophils, IgE | | |

| | | | |dependent platelets/mast cells | | |

| | | | |•Schistosomula susceptible to immune | | |

| | | | |attack | | |

|Schistosoma |•Same as above |•Affects GI Tract |•Same as above |•Same as above |•Same as above |•Same as above |

|japonicum | |•China, Japan, | | | | |

| | |Philippines | | | | |

|Schistosoma |•Same as above |•Affects Urinary Tract |•Same as above |•Same as above |•Eggs in urine, blood in urine|•Same as above |

|haematobium | |•Africa, Middle East | | |or bladder biopsy | |

|Schistosomal Dermatitis | |•Found in lakes |•Bird infective schistosomes |Swimmer’s Itch | | |

| | |throughout the world |•Humans are dead end hosts |•Rashes from cercaria boring into human | | |

| | | | |skin | | |

| | | | | | | |

| | | | | | | |

| | | | | | | |

•Human Cestodes - Tapeworms

|Parasite |Forms |Epidemiology |Transmission/ |Clinical Features |Diagnosis |Treatment |

| | | |Pathogenesis | | | |

|Characteristics of Cestodes |Adults –Attachment organ , scolex (four muscular suckers) w/ undifferentiated area behind the scolex. Chain |

|Life Cycle: 1. Adult worms always in the intestine |of segments behind scolex (proglottids) |

| |(Immature – Contain developing organs |

|2. Eggs or proglottids are excreted in the stool |(Mature – Contain male and female reproductive organs |

|3. Larval development always requires intermediate host |(Gravid – Contain eggs in the uterus |

|-Eggs are ingested by intermediate host ( grow to larvae | |

|4. Definitive host ingests intermediate host tissue w/larvae(Adults in intestine | |

|Taenia saginata |(Adult Worm |Definitive Hosts |Transmission |Taeniasis |Diagnosis and Differentiation |Prevention |

| |-Scolex or organ |(Humans |(Ingestion of raw or rare BEEF |•Adult tapeworm causes little damage |(Stool Specimen |(Cooking beef adequately |

|(Beef Tapeworm) |with 4 suckers |(Adult Attached in |containing cysticercus larvae |(Most infected pts are asymptomatic |(Morphology of gravid |(Prevent cow from consuming|

| |and grooves, no |Small Intestine |(Cattle ingest eggs contaminating|(GI complaints – sometimes vague |proglottids in stool sample |human feces |

| |hooks |(Worldwide w/high |grass or feed |(Migration or protrusion of proglottids |-15-20 uterine branches | |

| |(Immature |prevalence w/poor |}~~~~€??‚‚ƒƒ„„„„ƒ‚‚€}{xuqmjhghiknr|from anus |(Adult – No hooklets |Rx |

| |(Mature |sanitation and eating |v{ƒˆŠŒŽŽ??Œ‹‹‹‹Œ????‘“”••––———–•””| | |Niclosamide |

| |(Gravid |of raw beef |”““’‘??‹‰†ƒ€~{zxxwxxy{|}}}}|{ywusq|Cysticercus-Larvae go to small intestine | |zzzz{{||||}}}}}~~~~~~~~~~€?|

| |(Cysticercus | |pooopqrsuuvwxwxxxxxyyz{{{||||||||||and grow to adult worms | |?‚‚‚‚??€~}{ywutsstvxz}€‚„†‡|

| |-cystic structure | |||||}~€€?‚‚ƒƒƒ„„„„„„„…„ƒƒ‚€}zwsomj|-Usually only one adult tapeworm survives| |‡ˆˆ‰‰Š‹‹‹‹ŒŒ?Ž???‘‘’‘’‘‘•La|

| |contains fluid and| |ijkmptw{‚†ˆ‰Š‹ŠŠŠŠŠ‹‹•Ingestion of|and matures | |xative 1st to purge eggs |

| |single inverted | |EGGS | | |form intestine |

| |scolex | | | | |Paromomycin |

| |(Proglottids | |Life Cycle | | | |

| | | |Eggs or proglottids in | | | |

| | | |human⎝Ingestion by | | | |

| | | |cattle⎝cysticercus in BEEF⎝ | | | |

| | | |Ingestion of beef by human⎝Adult | | | |

| | | |worm in human intestineInIngestion| | | |

|Taenia solium |(Adult Worm |Definitive Hosts |Transmission |Taeniasis |Diagnosis and Differentiation |Prevention |

| |-Scolex or organ |(Humans |(Ingestion of raw or undercooked |(Same as above |(Stool Specimen |(Cooking pork adequately |

|(Pork Tapeworm) |with 4 suckers |(Adult Attached in |PORK containing cysticercus larvae|Cysticercosis |(Morphology of gravid |(Prevent pigs from |

| |and grooves, |Small Intestine |-Usually only one adult | |proglottids in stool sample |consuming human feces |

| |circle of hooks |(Predominant in | |Proglottids- Ingested, carried and |-5-10 uterine branches | |

| |(Immature |countries where |Life Cycle |disseminate in organs, EYES and BRAIN |(Adults – Circle of hooks |Rx |

| |(Mature |undercooked pork is |Eggs or proglottids in |•Space occupying lesion⎝seizures, | |Niclosamide |

| |(Gravid |eaten –Mexico, Latin |human†…„ƒ‚‚?€~}|{zyxwvvuuutttuuuuu|uveitis, retinitis, headache, vomiting | |Paromomycin |

| |(Cysticercus |America, Spain, |ttttuuuuuuvvvvvwwxxyyyyyzzz{||}}~~|•Disease dependent on locations and | | |

| |-cystic structure |Portugal, Africa, |€€€€€?????‚‚‚ƒƒƒƒƒƒ‚‚‚‚‚‚????€?€€€|numbers of cysticerci and host cell | | |

| |contains fluid and|India, SE Asia, China |???????????‚‚‚ƒƒ„„„……††‡‡ˆˆ‰Š‹‹ŒŒ‹|response | | |

| |single inverted |-Rare in U.S. |ŒŒŒŒŒŒŒ‹‹⎝Ingestion by | | | |

| |scolex | |pigs⎝cysticercus in PORK |•See below for more info | | |

| |(Proglottids | |⎝Ingestion of pork by human⎝Adult | | | |

| | | |worm in human intestine | | | |

| | | |(Eggs are infectious for humans | | | |

| | | |and may produce cysticercosis | | | |

|Taenia solium |•Egg |•Humans are all |•Source is always human |Cysticercosis |Diagnosis |Treatment |

| |•Embryo |accidental intermediate|•Ingestion of food or beverage |•Found in all tissues, esp. muscle, CNS, |•Clinical manifestations |Asymptomatic cysts and |

|Cysticercosis |•Cysticercus |hosts |contaminated with EGGS |eye and subQ tissue |•Exposure history |easily controlled seizures |

| | |•Nearly all infected pt|•Person w/infected ADULT may |•SubQ –stationary subQ masses |•CT and MRI Scans |do not need Rx |

| | |are immigrants from |disseminate eggs to others and/or |•Ocular-Occur in aqueous/vitreous humor |•Serology on serum and CSF |•Hydrocephalus – CSF |

| | |infected areas |cause autoinfection |and interfere with vision | |shunting procedures |

| | |•Infects all tissues |Life Cycle |•CNS-Cerebral cysticercosis | | |

| | | |Ingested Eggs hatch in intestine⎝ |1. Parenchymal cysts –Seizures, mass | |Rx |

| | | |Embryo penetrates mucosa |2. Meningeal involvement -Meningitis, CSF| |Niclosamide |

| | | |⎝Bloodstream⎝Site of |obstruction, Hydrocephalus | | |

| | | |development⎝Cysticercus |3. Intraventricular cyst -Hydrocephalus | | |

| | | | |•Spinal Cysticercosis – Spinal Cord | | |

|Parasite |Forms |Epidemiology |Transmission/ |Clinical Features |Diagnosis |Treatment |

| | | |Pathogenesis | | | |

|Echinococcus granulosus |•Eggs |Habitat |Transmission |Hydatid Disease |Diagnosis |Treatment |

| |•Hydatid Cysts |•Humans are accidental |•Ingestion of EGGS of parasite |•Hydatid cysts develop most frequently in|•Imaging techniques of |•Surgical removal of |

| |-Larva |intermediate hosts |from dogs (wolves, foxes, etc) |liver |ultrasound, CT scans and MRI |accessible cysts is |

| |•Adult Worm |•Sheep raising areas |•Eggs in dog feces contaminate |-other sites include: lung, brain, |•History of exposure |preferred |

| |•Embryo |•S. America, Africa, |environment⎝Egg ingested by |kidney, spleen, bone, heart |•Serologic tests-15% of liver | |

| |•Protoscolex |Mediterranean, Middle |sheep⎝hydatid cyst in sheep liver |•Cysts develop very slowly (1cm/yr) |cysts and 50% of lung cysts | |

| | |East, Central Asia, and|⎝Liver fed to dog⎝Adult worm in |•Symptoms due to mass, leakage or |may have negative serologies | |

| | |areas of Australia & |dog intestine⎝Eggs in dog feces |rupture, calcification (older cysts) |•Operation and finding hydatid| |

| | |New Zealand |ingested by human |•Liver Cysts – Pain when reach lg size |sand (protoscolices, hooks) in| |

| | |•Foci areas include CA,|⎝Hydatid cyst develops |•Lung Cysts – Asymptomatic and found on |fluid | |

| | |AZ, NM, Utah, Alaska | |chest X-ray | | |

| | |and Canada |•Humans are dead end hosts |•Hydatid Cysts – Can become infected with| | |

| | | | |2° bacterial infection | | |

Basic Mycology

Characteristics

•Fungi are Eukaryotic Organisms (bacteria are prokaryotes)

•Chromosomes, mitochondria, nucleus w/membrane

•Fungal Cell Wall – Complex Polysaccharides, chitin, glucans,

mannans, chitosan (bacterial walls are peptidoglycan)

(Insensitive to antibiotics such as penicillin that inhibits peptidoglycan

(These structural elements can be stained (See cell wall stains)

•Fungal Cell Membrane contains ergosterol and zymosterol (humans-cholesterol)

•Two Types of Fungi: Yeast and Moulds

Yeasts Moulds/Molds

•Unicellular •Multicellular

•Reproduce by budding/fission •Reproduce by germination of reproductive structure (into germ tube)

•Reproduction by budding is unique -Apical Extension (germ tube/filament grows from tip (apex)

•Colonies are soft and similar to bacteria -Continued extension results in hyphae or network of filaments

•Hyphae – 1) Septate 2)Nonseptate hyphae-coencytic or multinucleated

•Mycelium or thallus – Collection of hyphae in a cottony colony

Reproduction –Two major ways of reproduction, certain fungi may reproduce, one way or both ways

( Most fungi of medical interest reproduce asexually

ASEXUAL REPRODUCTION

1) Vegetative – Hyphae grow vegetatively and initiate new mycelium with transfer to new medium

2) Asexual Reproduction by Propagules – Anamorphic state and is accomplished by

reproductive propagules called conidia or spores depending on their mode of production

€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€€•Conidia - Asexual spores formed from ends/sides of structures

A. Arthroconidium-Thallic conidia that grow from entire

hyphae by germination and apical extension

B. Blastoconidium-Most yeast reproduce by blastic or budding process ⎝ O O

-Pseudohyphae – Blastoconidia sometimes do not separate at maturity but continue

to grow and elongate into sausage shaped filaments

C. Chlamydoconidium – Thick walled asexual unit arises by

thallic process

D. Macroconidium/Microconidium – Large and small conidia/spores

-Produced blastically and thallically

E. Sporangiospore – Spore produced by cytoplasmic cleavage w/in

a structure called a sporangium

SEXUAL REPRODUCTION

ƒ‚‚‚‚‚‚ƒ„…†‡‡ˆˆ‡†„‚?€~~}|zxvtrpomkigeca`aabcdfhjmqtx|€„ˆ?‘–™œž ¡¢¢£¤£££¢¡ Ÿ?›š—•“‘?•Some Fungi reproduce sexually by mating and produce sexual spores

-zygospores, ascospores and basidiospores

-not used in lab diagnosis

•Dermatomycosis-Fungal Skin Disease

|Parasite |Forms |Epidemiology |Transmission/ |Clinical Features |Diagnosis |Treatment |

| | | |Pathogenesis | | | |

|Dermatophytoses |•Ringworm |Anthropophilic – Only |Transmission |Ringworm/ Dermatophytoses |Direct Mount |Treatment |

| | |on humans w/dec. |•Direct Contact w/lesions or |•Involve ONLY the non-viable |•Scrapings of skin or nail |•Anti-fungal creams |

|•Epidermophyton | |conidiation |materials (hair, infected scales) |superficial keratinized layer of skin |placed in 10% KOH on a glass |•Oral griseofulvin |

|•Trichophyton | |Zoophilic – Mostly on |•Fomites – Infected material on |•Tinea – Diseases w/defined areas of |slide | |

|•Microsporum | |animals and |inanimate objects used by humans |involvement |-See hyphae w/microscope |-Ketoconazole |

| | |occasionally on humans |(toilet, door handle) |•Pruritic papules, vesicles, broken |-Patterns of arthroconidial | |

| | |Geophilic – Found in |•Materials Infectious up to 1yr |hairs, thickened, broken nails | | |

| | |soil | | |Ectothrix-hyphae surrounds the| |

| | | | | |hair shaft | |

| | | | | |Endothrix- hyphae within the | |

| | | | | |hair shaft | |

| | | | | | | |

| | | | | |Wood’s Light | |

| | | | | |Some Microsporum cause hairs | |

| | | | | |to fluoresce when exposed to | |

| | | | | |UV light (365nm) | |

| | | | | |•Usually tinea of cats/dogs | |

| | | | | | | |

| | | | | |Culture | |

| | | | | |•Culture on Sabourauds’s | |

| | | | | |Dextrose agar w/antibiotics | |

| | | | | |(chloramphenicol) and | |

| | | | | |anti-saprobic | |

| | | | | |mold(cycloheximide) at Room | |

| | | | | |Temp | |

| | | | | |•Growth of hyphae and conidia| |

|Tinea capitis | | |Very contagious |•Scalp and Hair | | |

|Tinea barbae | | | |•Chronic infection of bearded face/neck | | |

|Tinea corporis | | | |•Ringworm of glabrous/smooth skin | | |

| | | | |•Superficial scaling to deep granulomas | | |

|Tinea cruris | | | |•Jock Strap Itch –Ringworm of the groin, | | |

| | | | |perineum and perianal regions | | |

|Tinea pedis | | | |•Athlete’s Foot –Feet, toe webs, soles | | |

|Tinea unguim | | | |•Nails – difficult to treat | | |

Dermatomycoses Genera

|Microsporum |Trichophyton |Epidermophyton |

|Macroconidia |Macrocondia |Macroconidia |

|•Spiky |•Cylindrical |•Club Shaped |

|•Spindle Shaped |•Smooth |•Smooth |

|•Thick-walled |•Thin-walled |•Moderate Thick-walled |

|•Born singly (single) |•Born singly (single) |•Borne in clusters of two or three |

•Yeast Infections -Opportunistic Mycoses

|Parasite |Forms |Epidemiology |Transmission/ |Clinical Features |Diagnosis |Treatment |

| | | |Pathogenesis | | | |

|Candida |•Unicellular fungi|•Zoopthogenic sp. Are |Endogenous |Candidosis/Candidiasis |Diagnosis |Fluconazole |

|albicans |•Predominant |commensals of GI, |−Usually commensals with source of|•Acute or Subacute superficial | |Flucytosine |

| |Asexual |Vaginal and Oral mucosa|infection being endogenously |infection |Appearance in Tissue Exudates |Ketoconazole |

| |Reproduction | |precipitated by predisposed events|-Skin, nails and mucus membranes |– Yeast Cells (blastoconidia) | |

| |•Blastoconidium |•70-80% of all yeast |such as: |•Sometimes involve deep seated areas of |and hyphal elements | |

| |•Hyphae |infections |•Physiological Change |body |(pseudohyphae) | |

| |•Pseudohyphae | |-infancy, pregnancy | | | |

| | | |•Traumatic Changes |Cutaneous Lesions –Lesions resemble |Appearance in Cultures | |

| | | |-maceration (skin softened by |dermatophytes |•Soft, Cream colored colonies | |

| | | |moisture), post-operative infectxn|•Nail infection ⎝Clubbing around nail |of unicellular organisms | |

| | | |•Malnutrition |•Sites of accumulated moisture |(blastoconidia) | |

| | | |•Malignancy | |•Pseudohyphae | |

| | | |•Anemia |Mucous Membranes |•Germ tubes (C. albicans) | |

| | | |•Antibiotic or Immuno- |•Thrush –Recurrent |⎝true mycelium | |

| | | |suppressants |•Perleche – Corners of mouth due to | | |

| | | | |saliva accumulation |Germ Tube Test | |

| | | | |•Vulvovaginitis – Vagina mucosa, may be |•Emerse small portion of | |

| | | |EXOGENOUS |contagious |isolated colony in serum | |

| | | |Sexual Contact with Candida | |-Incubate at 37°C for 3hrs | |

| | | |infection |CMC- Chronic Mucocutaneous Candidiasis – |-Examine for germ tubes | |

| | | | |Pt w/immunological defects in CMI ie. |•Positive = C. albicans | |

| | | | |AIDS | | |

| | | | |•Repeated attacks, localized w/no spread |CMA- Corn Meal Agar | |

| | | | |to deeper organs or tissues |•Culture isolate on agar | |

| | | | | |•Produces pseudohyphae at room| |

| | | | |Systemic Disseminated Disease – Seen in |temp. | |

| | | | |advanced malignancies (bladder/ bowel |•Chlamydoconidia /vesicle | |

| | | | |cancer) or conditions with neutropenia |formed by C. albicans on CMA | |

| | | | | |•Creamy white colony | |

| | | | | | | |

| | | | | |Substrate Assimilation | |

| | | | | |•ID by assimilation pattern of| |

| | | | | |carbon sources | |

|C. glabrata |•Same as above | | | |•Does not form hyphae or | |

| |except: | | | |pseudohyphae | |

| |NO hyphae and | | | | | |

| |pseudohyphae | | | | | |

|C. guilliermondii |•Same as above | | | |•Forms reduced number of | |

| |except: | | | |pseudohyphae | |

| |REDUCED | | | | | |

| |pseudohyphae | | | | | |

|Cryptococcus |•SEE PULMONARY MYCOSES | | | | |

|neoformans | | | | | |

•Yeast Infections – Opportunistic Mycoses

|Parasite |Forms |Epidemiology |Transmission/ |Clinical Features |Diagnosis |Treatment |

| | | |Pathogenesis | | | |

|Cryptococcus |•Oval Budding |Habitat |Transmission |Cryptococcosis |Growth on Selective Media |Rx |

|neoformans |Yeast |•Worldwide |•Inhalation of infectious conidia |•Chronic, wasting, frequently fatal |•Biotypes can be distinguished|Ketoconazole |

| |•NOT Dimorphic |•C. neoformans var. |from exogenous source |disease |by physical attributes |Fluconazole |

| | |neoformans | |•CNS symptoms |•CGB medium |-meningoencephalitis |

| | |– Avian habitat |Anamorphic Form |•Often occurs in immunosuppressed pts |Tissue Stain | |

| | |(pigeon) |•Encapsulated yeast w/two biotypes|-AIDS (4th cause of death in AIDS pt) |•Blastoconidium in capsule | |

| | |-Only natural form is |-C. neoformans var. neoformans | |•India ink for visualization | |

| | |in debris from |(serotypes A and D) |Pulmonary Disease |in fluids | |

| | |Eucalyptus tree |-C. neoformans var. gattii |•Usually subclinical and overlooked | | |

| | |•C. neoformans var. |(serotypes B and C) |•Primary infection may disseminate |Culture | |

| | |gattii | |Disseminated Disease |•Mucoid colonies (looks like | |

| | |-Tropical and |Teleomorphic Form |•Meningitis |snot) w/ encapsulated yeast | |

| | |subtropical |•Sexual form of growth |•meninges and brain parenchyma common |cells seen w/india ink | |

| | | | |sites of spread |•Melanin deposits w/certain | |

| | | | |•Skin lesions occur in 20% cs of |catecholamines in growth media| |

| | | | |dissemination |(ie thistle seed agar) | |

| | | | | | |Diagnosis cont’d |

| | | | | | | |

| | | | | | |Serological Tests |

| | | | | | |•Latex Agglutination w/Ab |

| | | | | | |attached to beads |

| | | | | | |•CSF, Urine, Serum |

|Coccidioides immitis |•Dimorphic |Habitat |Transmission |Coccidioidomycoses |Dimorphism |Immunity to reinfection |

| |-MOLD mycelium/ |•Soil of arid or |•Inhalation |(Valley Fever) |•Room Temperature – mycelium |•(+) Skin test indicates |

| |hyphae |semiarid regions |•Not contagious from person to |•Primary infection – asymptomatic, |w/hyphae forming arthroconidia|previous infection and |

| |-SPHERULE |-alkaline soil, hot, |person |subclinical, self-limiting (60% pts) |(highly infectious) |immune to 2nd attack of |

| |spherules w/ |dry seasons, no frost | |•Pulmonary Disease w/various degrees of |•37°C consists of large |disease |

| |endospores |w/months of rain | |severity |spherules w/small endospores | |

| | |•New World organism | |-Influenza like, fever and cough - some | | |

| | |•Soil of North, Central| |lung cavitation |Tissue Appearance | |

| | |and South America | |-Erythema nodosum (10% of pts)-Red tender|•Endospore filled Spherule |Rx |

| | |•10-15% occur outside | |nodules on extensor surfaces ie. shin. |•Tissue or Exudates (CSF, |Fluconazole |

| | |endemic area (travel or| |(DTH rxn to fungal Ag) |Sputum, Pus) |Ketoconazole |

| | |shipped out) | | |Culture | |

| | |•CA – Kern, Tulare, | |Disseminated Disease |•Spherules hard to culture | |

| | |King and Fresno | |•Increased prevalence in non-caucasion |•Room Temp cultures used | |

| | |Counties | |population |Antibody Tests | |

| | |•AZ – Maricopa and Pima| |-( in Filipino population |•Ag – IgM,G,A,E classes | |

| | |Counties | |•Small % of pts ⎝chronic or acute |•Tube Preciptin Ab –IgM | |

| | | | |malignant disease that involves every |isotype early in symptomatic | |

| | | | |tissue and organ system in body |illness | |

| | | | | |•Complement Fixation Test (CF)| |

| | | | | |IgG Ab produced later in | |

| | | | | |infection ⎝titer | |

| | | | | |•Titer correlates w/severity | |

| | | | | |1:16 1° disease, 1:32 severe | |

| | | | | |*note: CNS sole area of | |

| | | | | |involvement titers are 1:16 | |

| | | | | |(low) | |

|Parasite |Forms |Epidemiology |Transmission/ |Clinical Features |Diagnosis |Treatment |

| | | |Pathogenesis | | | |

|Histoplasma |Facultative |Habitat |Transmission |Histoplasmosis |Appearance in Tissue |Ketoconazole |

|capsulatum |intracellular |•Soil contaminated |•Inhalation of spores and Mφ |•Asymptomatic and Subclinical (95%) |•Oval budding Yeast cells |-fungicidal and fungistatic|

| |parasite |w/bird droppings |engulf⎝develop into yeast form | |found in Mφ w/in tissue | |

| | |•Chicken, Starling and |•Not contagious from person to |Pulmonary Infection |-Tissue biopsy |Fluconazole |

| |Dimorphic |Bats (disease found |person |-Influenza-like, fever and congestion |-BM aspirates |-disseminated |

| |•Yeast |only in birds) | |•Cavitation of lung⎝Calcification of | |histoplasmosis |

| |•Mold |•Zoogenic (dogs, cats, |Dimorphism |small granulomatous foci in lung and |Appearance in Culture | |

| |Asexual Spores |mice, rats,etc can be |•Mold (saprophytic form) in |spleen |•Room Temperature-Hyphae and | |

| |•macroconidia |infected) |soil/Room Temperature |•Pneumonia |mycelium w/micro and | |

| |•microconidia |•Worldwide |-hyphae form w/mycelium | |macroconidia | |

| | |w/concentration in U.S.|-macroconidia |Disseminated Disease |-Microconidia are infectious | |

| | |-Ohio, MO, Missippi |-Infectious Element -Small |•Progressive and involves cells in : |•37°C converts yeast form | |

| | | |Spherical microconidia |Liver, Spleen and Lymph Nodes | | |

| | | | |•Hepatosplenomegaly |Serological Tests | |

| | | |•Ovoid budding Yeast (parasitic |•Usually immunosuppressed CMI and infants|•Complement Fixation (CF) | |

| | | |form) in tissue/37°C | |-titer of 1:32 | |

| | | |-blastoconidium | |-X-reactions occur (ie | |

| | | | | |Blastomyces) | |

| | | | | |•Immunodiffusion (ID) | |

| | | | | |-ppt Ab form 2 bands on agar | |

| | | | | |assay | |

| | | | | | | |

| | | | | |RIA’s | |

| | | | | |DNA/RNA Hybridization | |

|Blastomyces dermatitidis |Dimorphic |Habitat |Transmission |Blastomyces |Tissue Appearance |Pentamidine |

| |•Mold |•Moist, rich soil in |•Inhalation of conidia |•Pulmonary infection (1st stage) |Tissue Biopsy | |

| |•Yeast |organic material |•Not contagious from person to |-Asymptomatic or subclinical |•Large solitary yeast cells | |

| |-round w/ single |•Infects humans and |person |-Self-limiting, but ⎢ frequency than |embedded in abscesses w/single| |

| |broad-based bud |animals (note dogs) | |histoplasmosis and coccidioidomycosis |broad-based buds | |

| |•Conidia |•Worldwide distribution|Dimorphism |Chronic Infection |attached to mother cell | |

| | |•Males outnumber |•Mold at Room Temperature w/ |•Chronic infectio of skin w/suppurative |•Thick walls and not | |

| | |females 10 to 1 |mycelium and hyphae |granulomas that heal spontaneously or |intracellular | |

| | | |-Ovoid conidia (Infectious |w/therapy |-Sometimes seen in giant cells| |

| | | |Element) |-Foot, Leg and Face |Culture Appearance | |

| | | |•Yeast at 37°C – Blastoconidia |•Pronounced Scar formation |•White mycelium-hyphae | |

| | | |w/thick walls, wide base w/budding|•Indolent form – recurrent for many yrs |w/single lateral conidia | |

| | | |daughter cells | | | |

| | | |•Teleomorphic form of growth | | | |

•Opportunistic Fungal Diseases

|Parasite |Forms |Epidemiology |Transmission/ |Clinical Features |Diagnosis |Treatment |

| | | |Pathogenesis | | | |

|Aspergillus |Molds ONLY |Habitat |Transmission |Aspergillosis |Culture | |

|fumigatus |•conidia |•Grow on decaying |•Airborne Conidia |Allergic Bronchopulmonary Aspergillosis |•Fast growing, flat, velvety, | |

| |•conidiophore |vegetation |•Inhalation |•Induction of allergies (DTH) |bluish green colony | |

| |•septate hyphae |•Worldwide affecting |•Ingestion |•Asthmatic Symptoms –IgE mediated |•Brown w/aging | |

| | |all ages and sexes |•Abraded Skin | |•Physical appearance of chains| |

| | |•Immunocompromised | |Tissue Invasion |of enteroblastic phialoconidia| |

| | |Hosts | |•Infectious Invasion of Tissues |produced by one row of | |

| | | | |•Grow in lung ⎝pulmonary cavitation (from|phialides pointing upward from| |

| | | | |other disease processes, ie TB) |upper part of vesicle (in | |

| | | | |•Fungus Ball – seen on CXR |other words it looks like a | |

| | | | |•Hemoptysis and granulomas |Hairy Q-tip) | |

| | | | | | | |

| | | | |Toxin |Tissue Appearance | |

| | | | |•Toxins contaminate feed or food⎝ |•Septate hyphae that branch at| |

| | | | |Toxemia |acute angles | |

| | | | |•Grow on rice, cereals, nuts producing | | |

| | | | |aflatoxins that may be carcinogenic | | |

| | | | |and/or toxic | | |

| | | | |Disseminated Disease | | |

| | | | |•Immunocompromised Hosts | | |

| | | | |•Skin, CNS, heart, lung, nasal-orbital | | |

| | | | |area, cornea | | |

|Flavus | | | | | | |

|A. terreus | | | | | | |

|A. niger | | | | | | |

|Cryptococcus neoformans |See Pulmonary | | | | | |

| |Mycoses | | | | | |

|Candida albicans |See Yeast | | | | | |

|(sp.) |Infections | | | | | |

| | |

|*Note: Opportunistic Fungi fail to induce disease in most normal persons, but may do so in those with impaired host defenses | |

| | |

| | |

| | |

-----------------------

Cell Wall Stains

1) PAS – Periodic Acid-Schiff Stain

2) GMS – Gomori’s Methenamine Silver Stain

3) CF – Calcifluor Stain

Dimorphism

Many fungi grow in two morphologically distinct forms at different temperatures

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