Micro 2 Exam 1

Pseudallescheriasis

"ally's ass" Cause: -*Pseudallescheria (ally's ass) and Madurella (mad urine)* species are monomorphic molds that produce subcutaneous infections. All fungi known to cause *eumycetoma (fungal infection) (your rash, and my rash, on my ass)* belong to the *Phylum Ascomycota* although asci are not always produced. Epidemiology: Fungi are found worldwide in *soil, decaying vegetation, manure and polluted water (soil, vegetables, poop and water)* (reservoirs). Transmission is by inhalation or *traumatic implantation (bandage on patient)* of fomites into the skin. Pathogenesis: The incubation period is *months to years (show 365 days)* Hyphae invade subcutaneous tissues producing granulomas and develop into *allergic reactions (benadryl packet)* Organisms evade host defenses by depositing extracellular *melanin (melanie in corner of picture*), by forming thick cell walls and by *immunomodulation (immuno packet with knife through it - being modulated)* Subcutaneous infections lack the formation of granules when the patient has impaired immunity. Partial or protective immunity do not develop. Symptoms: Eumycetomas are characterized by *painless (smiley face)*, *tumor-like swellings (cells proliferating greatly)* in the skin that ulcerate, form sinus tracts and undergo fibrosis and scarring with a *woody disfigurement (picture of woody from toy story*) -Pulmonary pseudallescheriasis presents with bronchial pneumonia accompanied by bronchial colonization and *fungus ball formation (basektball)* Other forms include sinusitis, otomycosis, meningitis, arthritis, osteomyelitis, endocarditis, endophthalmitis, keratitis and cutaneous and subcutaneous lesions. Diagnosis: Stains of exudate reveal granules composed of *broad, branching septate (twig with many WIDE branches)* hyphae with dense, neutrophilic exudates occurring as *black grains (black wheat growing)*. Treatment: *Ketoconazole (a swole cone- cone with bicep coming from it)* is used for treatment. There is *resistance (stop sign)* to some azoles when there is a poor clinical response.

Tinea corporis

(Tinea of the body, facei and barbae are of the face) Cause: -*Microsporum, Trichophyton species and Epidermophyton floccosum (micro spores falling on head, tricholor (but on body), and flocks of birds flying above)* are monomorphic molds that cause cutaneous mycoses of the glabrous skin. -Epidemiology: Infection is found worldwide. -Transmission is person-to-person, by non-human mammals to people, by aerial dissemination or by fomites. -Pathogenesis: The incubation period is days to weeks. Hyphae or *conidia infect the horny layer (picture of man with horns)* of the skin and spread circularly. -The center of the lesion clears as the fungus is eliminated (center to borders). -Infection results in *partial protective immunity (PPI hat)* Symptoms: Tinea corporis produces rings of inflammation on the glabrous skin *of the body* that begin as dry and scaly patches which become pustular and crusty and can have *extensive hyperkeratosis (hypertrophy of the horny layer of the epidermis)* Two types are seen. 1) The *annular type*: -presents with small, spreading circular areas of erythema that become *scaly in the center with raised red margins* (red margins around scaly center). -Lesions *can become chronic* and form nodules. -*circular = chronic* 2) The *vesicular type*: -has vesicles and pustules behind the advancing erythematous border. -Lesions are usually not chronic. Diagnosis: -Stained preparations of scrapings reveal *mycelia and conidiospores (cones with walnuts for sale =sell)* Microsporum canis (canine- dogs and cats) has *club-shaped macroconidia with rough walls. (image: dog with club in hand and large macaroni, wall/gate to keep him in)* Treatment: *Terbinafine* (turbo scooter) is used for therapy.

Follicular acariasis

(allisa) A'Carra is a demon or EX foliation Cause: *Demodex folliculorum* (follicle mite) is an *arachnid (draw spider)* Epidemiology: Demodex folliculorum is a cosmopolitan (worldwide) mite found worldwide and has *humans only as reservoir and definitive hosts* (X through animals) Life Cycle: Adult mites are worm-like with a *short capitulum (draw short cap on patient)*, a *long tapering abdomen (draw long abdomen)* and very short legs. Eggs are laid, hatch into larvae and develop into adult mites on the infected person and can be transmitted directly to another person. Adult and larval stages are found living in the *hair follicles (draw redness on hair)* and *sebaceous glands (draw oil bottle)* around the nose, scalp and eyelids of humans and mammals. Pathogenesis: The incubation period is weeks to months. Mites infesting hair follicles of eyelashes and sebaceous glands can produce keratitis. Sebaceous glands infested on the forehead, eyelids, cheeks and nose can result in granulomas and secondary bacterial infections resembling acne. Infestations can be associated with *blackheads (draw black pimples on patient)* particularly in women using facial cream instead of soap and water. Partial or protective immunity do not follow infestation. Symptoms: Infestation rarely causes discomfort. Infestation associated with acne or blackheads usually does not cause inflammatory reactions unless secondary bacterial infections develop. *Excessive amounts of cosmetics (draw makeup bottles)* results in increased proliferation of mites in the dermis. Diagnosis: *Cigar-shaped mites TQ- patient smoking cigar* are found in follicle or skin scrapings. Treatment: *Lindane (draw jeremy lin)* is used for treatment.

Tinea capitis-endothrix

(main difference from ectothrix is endothrix occurs inside the hair shaft, ectothrix outside) Cause: -Trichophyton species are monomorphic molds that cause cutaneous mycoses of the scalp. Epidemiology: Trichophyton species are found worldwide and are transmitted person-to-person, by non-human mammals, by aerial dissemination and by fomites (same as ectothrix). -*Males have more infections than females (infects younger people more - before puberty)* Pathogenesis: The incubation period is days to weeks. -*Conidia are found inside the hair shafts with cuticular destruction* (difference from ectothrix) *(cones on head of patient not cups- for picture)* When the cuticle is involved, initial lesions are *small and angular* (holding protractor in hand) and are scattered over the scalp with variable inflammation that then develop into *erythematous circular lesions*. -Non-infective, cutaneous allergic eruptions occur along with *kerions* (K sticker, same as for ectothrix). -Infection results in partial protective immunity *(PPI hat)* Symptoms: Tinea capitis-endothrix, also known as *black-dot ringworm (man holding worm with black dots)* (big difference from ectothrix which was gray) , has erythematous, scaling, circular lesions with black dots that are broken off hairs. -Endothrix is a chronic infection that *can persist into adult life* -can result in hair loss. Diagnosis: -Conidia and hyphae are seen inside hair shafts on stained samples *(cones on top of mans head)* Treatment: Terbinafine is used for treatment (man on turbo- scooter).

Parasite pathogenicity

*Non-specific* host resistance to parasitism: *Chemical barriers*: Humans combat the invasion of parasites by secreting antiparasitic chemicals such as *acids* TQ of the stomach, skin and vagina, *bile salts* of the intestines and *lysozyme* in the eyes and saliva. Physical barriers: The intact skin, mucus on the lining of membranes, nasal hairs, cilia of the respiratory epithelium, *peristaltic movement* of the intestines and *normal microbial flora* prevent the entrance of parasites. Microbial antagonism: Antiparasitic factors in serum and the *competition for nutrients by normal flora** prevent parasite invasion. *Pathological changes* caused by parasites *Parenchymatous degeneration*: Damage to infected liver, cardiac muscle and kidney cells is characterized by *swollen cells packed with fatty granules* TQ, indistinct nuclei and *pale cytoplasm*. *Fatty degeneration*: Damage to infected liver cells results in deposition of large amounts of fat in cells imparting a *yellowish color to the cells*. *Necrosis*: Death of cells or tissues resulting from persistent cell degeneration gives the tissues an *opaque appearance* (muddy). *Hyperplasia*: An increase in cell numbers results from accelerated cell division producing an *elevated cell metabolic rate* due to an increase in host body repair activity that follows inflammation. *Hypertrophy*: An *increase in cell or organ SIZE* due to the presence of intracellular parasites. *Metaplasia*: *Conversion of one type of tissue into another* (without the intervention of embryonic tissue). *Neoplasia*: -Abnormal cell growth in a tissue producing an *entirely new structure such as a tumor* as the result of an attempt to repair an organ. -(Neoplasms may be benign (localized with no invasion of adjacent tissues) or malignant (invading adjacent tissues)).

Interactions of organisms in parasitism

*Obligate parasites* -cannot survive in a free-living state. *Facultative parasites* -normally have a free-living existence and establish a parasitic relationship with a host if the opportunity presents itself. *Endoparasites* -parasites that live inside their host. *Ectoparasites* -parasites that live on the outer surface of their hosts. *Definitive hosts* -hosts in which a parasite reaches sexual maturity and *reproduces* *Intermediate hosts* -hosts in which some development of the parasite occurs but does not mature. *Reservoir hosts* -*animals that harbor a species of parasite* that is also parasitic for humans and from which a human may become infected. *Vector hosts* -*arthropods or other living carriers that transport a pathogenic parasite* from an infected to a non-infected host. *Dead-end hosts* -organisms that harbor an intermediate life stage of a parasite but *do not transmit the parasite to another host* thus not allowing it to continue its life cycle.

Fungal cells have

*nuclei that are eukaryotic* with a *well-defined membrane* -mitochondria and an endoplasmic reticulum in the cytoplasm (like most eukaryotic cells). -a *bilayered cell membrane* -*the innermost layer* (around the cytoplasm) containing sterols, such as ergosterol, the essential sterol in fungi. -*a soft cell wall surrounding the cell membrane*, composed of (chitin, glucans, mannans, proteins, polysaccharides and glycopeptides that are) *recognized as antigens* (everything but sterols are on outside). -*a polysaccharide capsule* (coats and surrounds the cell wall) *in some yeasts*.

Taxonomy of fungi

-(Fungi of medical importance are assigned to four taxonomic phyla, depending on the mode of sexual or asexual spore formation). -*Fungi have asexual spores* -*can be single-celled or multicellular* -In Phylum *Ascomycota (the sac fungi)*, sexual reproduction results in an *ascus*, a saclike structure containing *four to eight ascospores* In Phylum *Basidiomycota (the club fungi)*, sexual reproduction produces *basidiospores* that are formed on a *club-shaped structure called a basidium* In Phylum *Zygomycota (the conjugation fungi)*, sexual reproduction takes place by simple copulation of the tips of multinucleate hyphae (no cross-walls) forming *large, thick-walled zygospores* that are *resistant to harsh environmental conditions* *Homothallic sexual reproduction* occurs when cells of a *single colony* engage in sexual reproduction. *Heterothallic sexual reproduction* occurs when *cells from two different colonies*, (+) and (-) hyphae, engage in sexual reproduction. -Fungi that reproduce *only asexually* (no sexual stage), producing *conidia*, are in the Phylum *Deuteromycota (Fungi Imperfecti)*.

Molds

-*hyphae grow by longitudinal extension* (and produce spores). -form *mycelia*- clumps of *intertwined, branching hyphae* -hyphae are divided into individual cells by *cross walls called septa* (septa have pores through which organelles can move from one cell to another). -*coenocytic hyphae: non-septate* with nuclei in a *continuous mass of cytoplasm*

Onchocerciasis (River blindness)

-centered around an onco-gene Cause: -*Onchocerca volvulus (onco-gene causing a volcano to errupt)* is an *arthropod-borne (draw mosquitto)* nematode. (River blindness) Epidemiology: Onchocerca volvulus is found in *Equatorial Africa, South and Central America (highlight these on map)* and has humans and *monkeys (draw monkeys next to volcano)* as reservoirs. *Black flies (draw flies that are black)* breed in *flowing rivers and streams (draw river/stream)* and are infectious 7 days after a blood meal. Life Cycle: Adult worms live in the subcutaneous tissues of *humans (definitive hosts)* and females release *microfilariae (small lab fillers)* into the skin and *lymphatic system (draw TI for thoracic inlet)*. Female black flies (Simulium species; intermediate hosts and vectors) pick up the microfilariae during a blood meal and the larvae develop into infectious *filariform larvae (filling up a water bottle)* Humans are infected when the black flies take a blood meal and filariform larvae are deposited in subcutaneous tissues becoming adult worms. *Microfilariae* are found in the skin after infection and humans can infect black flies for up to 10 to 15 years if untreated. Pathogenesis: The incubation period is *years (365)* Adult worms provoke a *fibroblastic reaction (show muscle fibers on dynamite)* in the subcutaneous tissues. Microfilariae cause *severe pathologic effects in the eyes (draw large red eyes)* when they die and become enveloped in a granuloma, a fibrous scar called an *onchocercoma* Partial or protective immunity do not follow infection. Symptoms: Subcutaneous *worm nodules (draw group of nightcrawlers joining at node)*, pruritic skin rashes, intraepithelial granulomas, interstitial keratitis or optic nerve damage result in blindness. Diagnosis: *Microfilariae* are seen in tissue nodule biopsies or skin snips. *Mazzotti Test (Maize rage)* - an oral dose of *diethylcarbamazine* produces a papular erythematous reaction in the affected skin along with conjunctival swelling. Treatment: *Diethylcarbamazine* is used for treatment.

subcutaneous mycoses: Chromoblastomycosis

-chrono watch, exploding (blasto) Cause: -*Cladophialophora, Fonsecaea and Phialophora (chad johnson/glad, the fonz, and fiez) species are monomorphic molds that produce subcutaneous infections. Epidemiology: The fungi are found in the *Americas, Africa and Japan* in *plant debris and soil* (reservoirs) (*plants in picture, map of america, africa and japan highlighted picture*) Transmission is by *traumatic implantation (bandages on patient*) of fomites into the skin. Pathogenesis: The incubation period is one *month or more (calendar with a whole month highlighted*) -Mycelial invasion of the subcutaneous tissues of the skin results in a *suppurative exudate (picture of soup)* with fibrous tissue forming *foci of necrosis (eyes = foci)* consisting of sclerotic cells in granulomas. A dense collagenous *encapsulation (show capsule around soup in picture)* of connective tissue forms around the fungi producing hyperplasia and granulomas with the *outer layer of skin becoming thickened and encrusted (show skin thick and crusty)* Partial or protective immunity do not follow infection. Symptoms: -*Verrucous dermatitis (patients name is veronica)* ( (warty proliferation of the skin) begins as papules, pustules and nodules in the skin of the *hands, feet and lower legs* and develops into *cauliflower-shaped lesions, TQ (show patient holding bind of cauliflower)* *Cladosporiosis (chad johnson/glad with spores)* is a condition that is characterized by single or multiple lesions in the *brain (walnuts (spores) falling on chads head and making him confused) causing cerebral headache, paralysis, coma or seizures. Diagnosis: -Stains reveal *sclerotic bodies (sclera of eye very large- for sclerotic) with *branching, septate (holding branching twig), brown hyphae (chad johnson playing for the browns) and thick-walled, round-to-oval brown cells with septa in infected tissue. Treatment: *Itraconazole (ezra in corner of picture with yamikah) is used as therapy.

Phaeohyphomycosis

-faith hill Cause: -Alternaria, Bipolaris, Cladophialophora, Exophiala, Scedosporium (chad johnson, alternative rock t-shirt, with magnet (bipolar), exit philia (loves exit signs), skidding)* species are monomorphic molds that produce subcutaneous infections. Epidemiology: The *dematiaceous (black) molds* are found worldwide in *plant debris, feces, soil and drinking water (show plants, feces, soil and water fountain) (faith hill pooping)* More than 100 species of *melanized fungi *patient is melanie)* have caused infection in humans and many of these are relatively rare as etiologic agents. The opportunistic molds are transmitted by *traumatic implantation (bandages on patient)* or *inhalation of conidia (inhaling cones)* These fungi are *typical opportunists (job wanted sign*) causing *infections increasing in severity in patients with impaired innate immunity or metabolic diseases (cane for immunocompromised)* Pathogenesis: The incubation period is weeks. -*Multiple granulomatous abscesses (patient with strong abs*) (fibrous capsules) are formed in tissues surrounding swollen, *oval hyphae (branches with oval top and bottoms)* and *conidia and have necrotic centers (cones with red/necrotic centers)* Partial or protective immunity do not follow infection. Symptoms: Cutaneous phaeohyphomycosis presents as *cracked, fissured (large fissure in middle of picture)*, ulcerated, *lichenified (tongue out and licking)*, eczematous skin around the *lower or upper limbs*. Phaeomycotic cysts are *asymptomatic (asymptomatic hat), solitary (playing game of solitaire*), well-encapsulated subcutaneous nodules. -Cerebral phaeohyphomycosis is an infection of the brain that results in CNS signs. Diagnosis: -Stains reveal dense masses of *branching, septate (twig with branches*), *brown hyphae (browns jersey*) and pigmented conidia in infected tissue. -*Melanin (melanie)* in cell walls is the pigment producing the color. Melanized yeast-like cells can also occur. Treatment: *Miconazole (jumpman 23)* is used for therapy. *Resistance (stop sign)* is seen against most azole drugs.

Acanthamoebic keratitis

-hitting the can (pooping) in Moab/Utah. Cause: *Acanthamoeba castellani* is a *non-arthropod (mosquitto/fly with X through it)*-borne amoeba. Epidemiology: Acanthamoeba castellani is found worldwide and is ubiquitous in *air, soil and water (gusts of wind = air)* and is an accidental human infection. Life Cycle: -In *fresh water*, Acanthamoeba castellani multiplies as amoebas forming *cysts (Kris *) that persist and revert back to amoebas that live in micro-environments in the soil. The amoebic and cystic forms enter damaged tissue in the eyes, lungs, skin or uterus of humans following exposure to soil, swimming, *hot tubs, sewage systems (picture of hot tub and sewage system supplying it)*, cooling towers or contact lens solutions. -Disease is commonly found in 30- to 50-year-old patients. Pathogenesis: The incubation period is days to weeks. *Commensal (person pooping is benefited but hot tub is not)* bacterial co-infection on the *eyelids and conjunctiva* play a role in the establishment of disease. *Collagenase and proteolytic enzymes (college to pro trasnition)* are released by amoebas. A characteristic stromal infiltrate in the shape of a *complete or partial ring develops in the eye (person wearing ring)* followed by a recurrent breakdown and healing of the overlying epithelium. Immune activation of neutrophils by lymphokines and opsonization of the ameba by antibody promotes an antibody-dependent cellular reaction. Partial or protective immunity do not follow infection. Symptoms: *Uveitis* (UV light- inflammation of the iris and ciliary body), *optic neuritis* (inflammation of the optic nerve) or corneal keratitis (inflammation of the cornea) occurs following infection. Granulomatous amoebic encephalitis develops in immunocompromised patients and presents with *fever, headache and seizures (patient with fire over head- for headache and fever*) *Acanthamoeba skin lesions* occur months before invasion of the brain and present as ulcers, nodules, abscesses and amebic granulomas. Diagnosis: Demonstration of amoebas or *star-like cysts (stars in sky)* in stained smears of tissue exudates. Treatment: *Propamidine (patient drinking propel)* is used successfully as therapy.

Lobomycosis

-image is rebecca lobo (tall girl with basketball). Cause: -*Lacazia loboi* is a monomorphic yeast that produces subcutaneous infections. Epidemiology: Lacazia loboi is found in *South, Central America and Florida (map highlighting florida, central and south america)* as an infection of humans and *dolphins -TQ- (dolphin in picture)* (reservoirs). It is transmitted by *traumatic contact (bandages*) with the skin. Pathogenesis: The incubation period is one month or more. -Yeast cells in the skin release *toxic compounds (*toxic danger sign*) that produce a pronounced inflammatory reaction leading to chronic granulomas. Partial or protective immunity do not follow infection. Symptoms: *Painless, plaques and keloids (smiley face, teeth with plaque and K for keloids*) on the skin eventually ulcerate, spreading to form *large tumor-like areas (large T on chest*) of infection. Squamous cell carcinomas can develop in chronic lesions. Diagnosis: Stains of tissue show thick-walled, globose-to-*lemon-shaped (draw yellow lemon*) budding yeasts joined by short tubes (*group of plumbing tubes*) (chains of yeasts). This yeast cannot be cultured. Treatment: Treatment is *surgical excision (knife and mask for surgery*)

Tinea manuum

-infection of hands- *men/man uses hands for work*) Cause: *Epidermophyton floccosum, Microsporum and Trichophyton (flocks of birds, micro-spores/walnuts falling, and tricolor on HANDS) species are monomorphic molds that cause cutaneous mycoses of the palms and fingers. Epidemiology: -Molds are found worldwide. -Transmission is person-to-person, by aerial dissemination and by exposure to contaminated fomites. -Disease is *most prevalent in males, usually associated with Tinea pedis (man with young child (pedis))* (usually affecting people before puberty) Pathogenesis: -The incubation period is days to weeks. -Infection begins when there is *maceration (maze spray)* of the skin due to *occupational activities*. -Infection of the palms and fingers results in lesions that begin as exfoliative, erythematous, scaly sheets of skin that *become vesicular, red circumscribed patches* -Infection results in partial protective immunity (PPI hat) Symptoms: -Patients have diffuse hyperkeratosis of the palms and fingers with concentric exfoliation of the skin. Vesicular circumscribed patches, discrete red papules and follicular patches and erythematous scaly sheets develop on the *dorsum of the hand (dorsal fin). (top of hand, non palm). Diagnosis: Stained preparations of skin scrapings show masses of hyphae and *macroconidia (macro pieces of macaronni*) Treatment: *Miconazole is used for therapy (Man holding microphone)*.

Candidiasis

-infection of the mouth -(picture centered around canadian) Cause: *Candida albicans* and other species of Candida are monomorphic *opportunistic yeasts (jobs offered sign*). Epidemiology: Candida species are found worldwide as normal human gastrointestinal, skin, oropharyngeal and vaginal flora and are transmitted by person-to-person contact, *nosocomially (jobs sign on hospital window)* or by contaminated fomites. Pathogenesis: The incubation period is days. *Gelatinous (jelly like- patient is trapped in jelly)* types of lesions develop when masses of fungi present with a mucoid degeneration of the invaded tissue resulting in *large emboli (girlfriend emily for emboli)* in the brain, spleen and kidneys. *Farnesol (travel to US for canadian to find job in hospital- have a FAR travel ahead)* influences the fungus' transitions between the noninvasive yeast and the invasive hyphal morphologies. *Granulomas (holding one grand in hand)* contain fungal cells in leukocyte-packed tissue. Allergic reactions can develop, however partial or protective immunity do not follow infection. Symptoms: Mucocutaneous candidiasis (thrush) presents as *glossitis (glossy/shinny teeth)* -(white to gray pseudomembrane covering of the tongue), -stomatitis (punctate, raised patches with commissural folds on the tongue) *(stoma = stem of plant which is like tongue)* -cheilitis (erosions over the lips) (*chilli on the lips and hot, erods)* -perleche (cracking lesions in the corners of the mouth) (*per=perimeter, lesions around mouth and in corners*) -vaginitis, balanitis (infection of the penis), gastroenteritis and bronchitis in neutropenic, immunocompromised patients. Cutaneous candidiasis can occur intertriginously or in a generalized fashion, and causes *paronychia (finger nails are swollen- big blob of red on them)*, diaper rash (*baby crying*) , *onychomycosis (onyx*) or candidal granulomas. Systemic candidiasis produces fever, headache, anorexia, myalgia, arthralgia, urinary tract infections, heart murmur, hepatosplenomegaly, hematuria, endocarditis (after cardiovascular surgery), heart valve replacement and meningitis can be induced iatrogenically following the prolonged use of *antibiotics or is associated with narcotic addiction (*pill bottle next to patient)* Diagnosis: -Exudates of infected tissues or blood have chains of *oval-to-globose, budding yeast cells (*large globe in picture) or pseudohyphae (*man holding a branch he named sue*) with constrictions at septa and with *oval blastospores (dynamite = boom in picture*) near the septa. Treatment: *Fluconazole or amphotericin B (thermometer in mouth b/c has flu or pho soup)* is used as therapy.

Onychomycosis

-ony, the onyx fungi (picture centered around onyx) Cause: -*Arthroderma, Aspergillus, Candida, Geotrichum and Scopulariopsis* are monomorphic opportunistic mold and yeast species. Epidemiology: These fungi are found worldwide in soil and as normal human flora. They are transmitted by implantation with spore-contaminated fomites. -*Nail infection (onyx has nails that are infected)* often accompanies a disseminated disease that causes the patient to be immunosuppressed. Pathogenesis: The *incubation period is unknown (question mark*) Infection of the nail results in damage to the nail architecture with *inflammation of web spaces (onyx feet also has redness between toes)* Partial or protective immunity do not follow infection. Symptoms: Finger or toenail plates develop grooves and cavities that accumulate debris but without thickening of the nail plate. Lesions are *painful (onyx saying oww)* and pigmented with brittleness of the nails. Diagnosis: Various forms of hyphal elements- *branching or non-branching hyphae (onyx holding one twig with branches, other without)* or pseudohyphae are found in scrapings of skin or nails. Treatment: *Itraconazole (ezra in bottom corner with kippa) is used for therapy.

Leishmaniasis

-person on leash Cause: The *Leishmania braziliensis complex, Leishmania donovani complex, Leishmania mexicana complex and the Leishmania tropica* (Patient is Donovan - muscles or crossfit T- map of Brazil, Mexico, Tropics), an complex are *arthropod-borne flagellates (show mosquttio) (show donovn with tail) Epidemiology: -Leishmania *tropica and donovani complex is found in Africa, Asia and Europe, donovani also in south america (tropics = Africa, Asia and Europe, donovan traveling to S. America)* -*Leishmania braziliensis and Leishmania mexicana complexes in Central and South America* with humans and non-human mammals as reservoirs and intermediate hosts. Leishmaniasis is transmitted by direct contact with infected tissue, by *blood transfusions (have blood donation bag) and *congenitally from mother to child (TORCH- have fire torch)* Life Cycle: Parasites are found in *nocturnal biting female sand fly (female sign over fly with moon for night)* vectors (Phlebotomus species, reservoir hosts) that *ingest macrophages containing the amastigote (macrophage sign on goat)* stage while taking a blood meal from an infected person or animal. Amastigotes develop into promastigotes in the sandflies and are then injected into a new host during a blood meal. Promastigotes enter the macrophages of the new host and develop into intracellular amastigotes that multiply in tissues producing lesions. Pathogenesis: The incubation period is weeks to months for the cutaneous forms and weeks to years for the visceral form. -Infiltrations of lymphocytes and plasma cells result in hyperkeratosis, necrosis and *ulceration (large U for ulcerations)* of skin or mucous membranes. -L. donovani amastigotes are distributed throughout the *reticuloendothelial system (R on skin)* by macrophages and invade visceral organs. Protective immunity is limited to the species causing the infection (so none or humans). Symptoms: Infection with Leishmania tropica results in the formation of papules, nodules, *ulcers and scars (U for ulcers and lighting for scars on body)* on the skin. Infection with Leishmania braziliensis and Leishmania mexicana produce *ulcers* on the skin and also infect the mucous membranes. Symptoms of Leishmania donovani include fever, *edema (E for edema)*, anemia, diarrhea, weakness, conjunctivitis, keratitis and *photophobia (sunglasses)* Diagnosis: Biopsies of bone marrow, spleen, liver or skin lesions show intracellular *amastigotes (draw goats)* on stained smears. Treatment: *Antimony sodium gluconate (sodium candy bar/glucose)* is used for treatment.

Rhinosporidiosis

-picture centered around rhino Cause: -*Rhinosporidium seeberi (rhino with a light saber*) is a monomorphic mold that produces subcutaneous infections. Epidemiology: -Rhinosporidium seeberi is found worldwide in *soil and water (rhino over soil and water)* (reservoirs). It is transmitted by inhalation or by contact with stagnant fresh water. Pathogenesis: -The incubation period is not known. *Micro-abscesses or a polyps (small abs on rhino) (poly high school jersey)* (bulging masses of tissue) develop due to the establishment of the mold infection in the mucosa of tissue. Lesions contain *globular sporangia (spores in a globular shape*) filled with endospores producing granulomas. Partial or protective immunity do not follow infection. Symptoms: Nasal rhinosporidiosis presents as *sessile (seeds)* or pedunculated *polyps (poly football jersey)* that develop in the mucous membranes of the *nose and palate (rhino -> big nose)* Ocular rhinosporidiosis is characterized by *sessile or stalked growths (large bean stalk coming from eye*) in the conjunctiva. Cutaneous rhinosporidiosis presents as *wart-like (warts on skin, W's)* ulcerated cutaneous lesions. Systemic rhinosporidiosis presents as *polyp*-like growths in bone, liver, lung, spleen or brain. Diagnosis: -Stains of biopsied infected tissues show *thick-walled spherules (thick walled spheres surrounding rhino)* (sporangia) with endospores inside. This fungus has not been cultured in the laboratory. Treatment: Treatment is with *amphotericin B (bowl of pho soup with letter B inside)*

Tinea cruris

-tinea of the groin area (cruel b/c goes after groin) Cause: -*Epidermophyton floccosum and Trichophyton (flocs of birds and tricolor on the GROIN*) species are monomorphic molds that cause cutaneous mycoses of the groin area. Epidemiology: Fungi are found worldwide with *humans as reservoirs* They are transmitted person-to-person, by aerial dissemination or by fomites. *20 to 30-year-old males (post puberty, baby with armpit hairs*) are more commonly infected than females. -(age where boys wear jock straps) *Tinea cruris is often associated with tinea pedis* Pathogenesis: The incubation period is days to weeks. Hyphae invade the moist areas of the groin and perianal areas causing *erythematous, edematous lesions* Infection results in *partial protective immunity* (PPI hat). Symptoms: Tinea cruris, commonly called *jock itch* TQ , begins as circular lesions in the groin and scrotum areas and develops into *serpiginous (serpent/snake around waist)*, well marginated, erythematous lesions with raised borders containing *tiny vesicles (serpant with tiny diamonds on it). Erythema and intense itching occur at first with older lesions becoming *leather-like (leather boots)*. Diagnosis: -Stains reveal hyphae and *conidia - (cones on head)* -Epidermophyton species have *club-shaped macroconidia (macro macaroni with club maraccas)* with *smooth walls (tricholor groin patient is trapped in walls- touching bc smooth)*. -*Trichophyton only produces microconidia (tricolor groin with micro macaronni)* Treatment: *Terbinafine (turbo scooter)* is used for treatment.

Tinea unguium

-tinea of the toenails (unguim = nail) (yum the toenails) Cause: -*Epidermophyton floccosum and Trichophyton (flocking birds above and tricolored on TOENAILS)* (no microsporum like in corporis) species are monomorphic molds that cause cutaneous mycoses of the nail plates. Epidemiology: -Organisms are found worldwide. -They are transmitted person-to-person, by aerial dissemination or by fomites. Incidence of infection is *greatest in males after puberty* (hair on legs/feet helps spread fungi via sweat) (*show boy with pit hairs*) (females get pedicures so more clean). Tinea unguium is usually *associated with Tinea pedis or Tinea manuum* Pathogenesis: The *incubation period is unknown (question mark sticker* on man with nail tricholor) -Nail injury predisposes to infection. -Tinea unguium starts in or under the nail plate of the *fingers or toes* Hyphae growing out of the nail plate *into the stratum corneum* (all tinea) produces inflammation by releasing enzymes that interact with skin and nail proteins. Patients develop a *partial protective immunity (PPI hat)* after recovery. Symptoms: Tinea unguium produces soft, friable, keratin that loosens the nail and *thickens the plate of fingernails or toenails*. -*Leukonychia mycotica (tic on nail*) is nail invasion restricted to *white patches or pits on the surface of the nail* (lekuo = white, nychia = nail). Invasive *subungual dermatophytosis* occurs when the lateral or distal edges of the nail are first involved and develop into a *nail plate that is brittle, friable and thickened with cracks and are brown or black in color* Diagnosis: Hyphae and *macroconidia (large pieces of macaroni) are seen on stained preparations. Treatment: *Terbinafine* (turbo scooter) is used for treatment. -Most infections are *very resistant (security guard halting scooter)* to treatment and become chronic, life-long infections.

Examples of vegetative mold structures

1) *Favic chandelier structures*: are (multiple branched hyphal ends that resemble reindeer antlers or chandeliers). 2) *Knotted hyphae* consist of closely twisted, entwined hyphae forming nodular structures. 3) *Pectinate bodies* are hyphal projections that look like *broken combs* (massive pecs brake comb) 4) *Racquet mycelia* are hyphae that consist of a chain of segments, each piece with an enlarged end, giving an appearance of a *chain of tennis racquets* 5) *Spirals or coiled hyphae* are *bedspring-like* helical coils that are found at the *ends of hyphae*.

Examples of asexual spores of molds

1) Arthrospores: -hyphal segments that are formed by the *fragmentation of hyphae* 2) Chlamydospores -*thick-walled spores* that are formed *terminally or within hyphal segments* 3) Conidiospores -formed at the *tips of hyphae* and are known as *microconidia if they are small* (and unicellular) or *macroconidia if they are large* (and contain more than one spore). 4) *Sporangia are spherical*, sac-like structures containing *sporangiospores* (sporangia for spherical or sac) (Some fungi produce only one kind of asexual spore and others up to four different morphological forms).

Phylum Arthropoda - Arthropods

1.Adult arthropods have segmented, *bilaterally symmetrical bodies (draw line through patient to show symmetry)* and range from *1 millimeter to 5 centimeters* in length (smaller than nematodes, cestodes, and trematodes/flukes). 2. The exoskeleton is an external rigid tegument of *hard plates* connected by *flexible, chitinized membranes (setting in Chi town)* 2.a. Exoskeletons are divisible into a *head, thorax and abdomen in Class Insecta*; Class *Arachnida have a fused head and thorax* (cephalothorax). 2.b. Arthropods may contain *cephalic, multi-jointed appendages* including *antennae* TQ, compound or simple eyes, or *chewing or biting mouthparts* TQ (like humans/animals). 2.c. Adult arthropods have *three (insects) or four (arachnids) pairs of legs* 2.d. (Insects are mosquito-like animals with or without wings) 2.e. (Arachnids are spider-like animals without wings) 3. Arthropods have a digestive system that consists of a foregut composed of a pharynx, esophagus and *proventriculus (show heart with ventricle)*, a stomach or midgut and a hindgut, intestine, *rectum* TQ and anus. 4. Arthropods grow by *molting (show volcano)* TQ either by *incomplete metamorphosis* (egg to nymph to adult) *or complete metamorphosis* (egg to larvae to pupae to adult). 4.a. Intermediate stages coexist with adults in or on host tissues or live independently. 5. Arthropods have *separate sexes (dioecious) (show patient with only penis)* and are *oviparous (release eggs), viviparous (release live larvae) or ovoviviparous (release larvated eggs)* TQ

Cutaneous Mycosis: Otomycosis

Cause: *Aspergillus, Penicillium, Mucor and Rhizopus* (asthma, with mucus and rhinovirus use penicllin), species are opportunistic, *saprophytic*, monomorphic molds that cause superficial infections of the *outer ear* TQ (otto = ear) Epidemiology: -The disease is *found worldwide* (everyone gets ear infections) in soil and infects humans and animals but *humans and animals are not reservoirs* (get from SOIL) - (find ears in soil). -transmitted by contact with contaminated *fomites* (like all above). Pathogenesis: The *incubation period is days* (like all above). Infection results in an accumulation of large masses of epithelial debris containing *fungi and/or bacteria* (creates secondary infections) and fungi in the external auditory meatus. -Partial or protective immunity do not follow infection (can get ear infections many times in life). Symptoms: *Otomycosis* is a chronic infection of the external ear characterized by *itching, pain, inflammation, loss of hearing and serous secretion*. Diagnosis: -Stained preparations of exudate reveal *fragments of mycelium, with or without branches* and septa. (ear infections can be hiding out without projections - latent). -*Conidiophores and conidia* or *sporangiophores and spores* may be seen. (*spores*- same as white piedra -> spreads easily around ear). Treatment: *Ketoconazole* (treats cone of ear) is used for treatment and a wax hook to remove exudate.

Tinea nigra

Cause: *Hortaea werneckii* (horton = black, nigra = AA have wernikes aphasia) is a *black, dematiaceous (means black; demons are black), monomorphic mold* that causes a superficial mycosis of the skin. Epidemiology: Hortaea werneckii is found worldwide in stagnant *water and soil* and is normal flora of humans and non-human mammals (same as white piedra) (get this if swimming in lakes or playing in dirty areas) -(Transmission is by person-to-person or non-human mammal-to-person contact or by contact with contaminated fomites). Pathogenesis: The *incubation period is days* (medium) The mold *feeds on the stratum corneum* (same as tinea versicolor) layer of the *hands and feet* resulting in a squamous cell turnover of the outer epithelium. -(Partial or protective immunity do not follow infection) (same as all above). Symptoms: *Solitary, brownish-black*, -*non-scaly (unlike verisicolor), flat*, painless macules mottled with *deeper pigmentation form at the advancing periphery* Diagnosis: -Staining of skin scrapings shows *multiple-branched septate*, dark pigmented hyphae and *elongated, budding cells* (AA are very buddy-buddy and have many kids - multiple branches) -Lesions must be differentiated from malignant melanoma or contact dermatitis. Treatment: *Miconazole* (ole = steroid blockage) is used for treatment.

Bed bug infestations

Cause: *Cimex lectularius (lecture on climaxing in bed)* is the bed bug, a *wingless insect (draw fly without wings)* *Bed bug infestations (draw bed with many bugs on it)* Epidemiology: Cimex lectularius is found worldwide and has humans and non- human mammals as reservoirs. Temperatures *above 98 F or under 5 F are lethal* to bed bugs. Life Cycle: Adult bugs *suck blood from sleeping humans (bugs with red straw)* The bugs lay eggs in bedding and in the *cracks of walls (draw slashes in wall)* where *incomplete metamorphosis (half baby half adult)* occurs producing nymph stages that develop into adult bed bugs. Nymph stages and adults take blood meals by piercing the skin with their *elongated beaks* (blood meals are required between each of five molts). Habitual harborage sites are marked by *brown or black spots of dried blood (draw these on the bed)* on surfaces where bugs rest, such as bed sheets, clothing or on human skin. Bed bugs possess *stink glands and emit an odor (have smelly odor coming from bed)* Pathogenesis: The bed bug life cycle requires four weeks to go from eggs to adults. Bed bugs feed exclusively at night and feed every few days. When nymph or adult bed bugs suck blood (they have piercing-sucking mouthparts), they inject substances just below the surface of the skin that are lytic compounds that also act as allergens producing *allergic responses (benadryl)* and lesions at the site of the bite. *Several bites in a row or tract- TQ (patient has bites in series on arm)* are characteristic of infestation. Partial or protective immunity do not follow infestation. Symptoms: Bed bug bites produce white to red, itching hard welts that *develop into sores (sour candy)* at the bite sites. Allergic responses may produce granulomas, hemorrhagic *bullae (draw bull)* or secondary bacterial infections can occur. Diagnosis: A history of contact with the insects or capture and identification of the involved organism. Treatment: *Steroids* are used as therapy.

Tinea pedis

Cause: -*Epidermophyton floccosum and Trichophyton (flocks of birds and tricholors on TOES)* species are monomorphic molds that cause cutaneous mycoses of the feet. Epidemiology: Tinea pedis (athlete's foot) is found worldwide and is the *most common fungal infection of humans (reservoirs) (were #1 fan finger)* It is transmitted person-to-person, by aerial dissemination or by fomites and is *most often seen in adult males* and is *rare in individuals that habitually go barefoot* (b/c trap less sweat). The organisms are frequently found in moist environments such as *pool decks and shower rooms (patient taking shower*). Pathogenesis: The *incubation period is unknown (question mark sticker)* -A breakdown in the host's skin defenses promotes the invasion of the epidermis by hyphae. -Infections are *localized to keratinized skin* Chronic, *papulosquamous (squash for squamous)*(with both papules and scales) and hyperkeratotic (overgrowth of cells) skin is seen. There is a poor cell-mediated immune response to the infection that does not result in partial or protective immunity. Symptoms: Tinea pedis, commonly called athlete's foot, presents as an itching, chronic, *intertriginous* (skin rubbing against each other) dermatitis with peeling, *maceration (softening) and fissuring (furrowing)* of the skin intertriginous between the *third, fourth and fifth toes (3, 4, 5, staying alive sign)*. A vesicular form with *vesicles or bullae (bull coming out of toes)* (blisters full of clear serum) on the *dorsal surface of the foot (dorsal fin)* that ulcerate and secondary bacterial infections develop. The patients often also have infections on their fingers Diagnosis: -Stained preparations reveal hyphae and macro- or microconidia (mix of macro and micro macarroni*) Treatment: Terbinafine (turbo scooter) is used for treatment.

Pityriasis (tinea) versicolor

Cause: -*Malassezia furfur* (malassezia- itallian flag is many colors) is a *lipophilic, dimorphic* (itallian food - two types- pastas and pizzas- creates lots of fat) fungus that causes a superficial mycotic infection of the skin. Epidemiology: Malassezia furfur is found *worldwide as normal flora* of humans and non-human mammals. -(transmitted by person-to-person contact, non-human mammal-to-person contact or by contact with contaminated fomites). -(Predisposing factors are the *use of lipid emulsions*, illness, malnutrition, high cortisol levels and high temperature and humidity). -*Incidence rates are medium*: 40 to 60%. -Infections are most common between *adolescence and middle age* (high in teenagers -> white pigments on skin - annoying problem like acne) and there is a *genetic susceptibility* (none in piedra). Pathogenesis: The *incubation period is days* (medium). -Superficial skin infections occur when this *lipophilic* TQ TQ (fatter people get this more) fungus feeds on skin oil and *removes the stratum corneum layer* TQ TQ resulting in a squamous cell *turnover of the outer epithelium* (outer layer of cake bit off). -(Partial or protective immunity do not follow infection) (none have so far). Symptoms: Pityriasis versicolor lesions are -*red/brownish, blotchy/scaly TQ*, -painless, *hypopigmented or hyperpigmented patches* on the skin of the upper body of non-suntanned individuals. -*Suntanned and dark-skinned people have pinkish-white patches* (b/c must contrast, so if darkened will be light) on the skin of the upper body. -Infection can develop into *itchy papules and pustules* (causes sweating/itching - nervousness symptoms), (inflammation of hair follicles or the lacrimal sac) or atopic dermatitis on the back and upper trunk. Diagnosis: -Staining of skin scrapings show *short, stubby hyphae* and globose budding yeast cells in the form of *spaghetti and meatballs* TQ -> (itallian food scene) Treatment: *Ketoconazole* is used for treatment ("ole drugs" - inhibit steroid synthesis/loss of membrane stability).

Tinea capitis-ectothrix

Cause: -*Microsporum* (show micro spores - walnuts) falling on head)) species are monomorphic molds that cause cutaneous mycoses of the *scalp*. Epidemiology: -*Tinea capitis-ectothrix* is found *worldwide* -*Tinea favosa* is found in *Africa and Europe* (map showing Africa and Europe) -Humans and non-human mammals are reservoirs. -Infection is transmitted person-to-person, by non-human mammals, by aerial dissemination and by fomites. -*Male infections are more common before puberty and females are mainly infected after puberty* -(infect females via menstruation, male testosterone fights off the bug) (the cougar more susceptible, cougar in Africa) Pathogenesis: -The incubation period is days to weeks. -Hyphae proliferate in the *stratum corneum* (like all tinea), the hair follicles and on the *outside of hair shafts* (with piedra it was along the hair shaft). -Infection results in *partial protective immunity* (PPI hat on man with scalp infection) Symptoms: Tinea capitis-ectothrix, also known as *gray-patch ringworm TQ TQ (man holding gray worm on hand*) is a *prepubertal (in males) infection of the scalp, eyelashes and eyebrows (glitter on eyelashes, eyebrows)* -*Infected hairs have a pale, scaly, grayish, Lusterless* appearance and *break off*. -Lesions begin as coalesced papules in a *ring form* and can develop into *kerions* (boggy areas of massive inflammation) *or keloids* (scars produced by collagen deposition) (bald man with large K sticker on chest (for keloids)). Allergic reactions producing *dermatophytids* (small vesicles) can occur. *Itching is severe (patient itching himself*) -tissue damage can lead to *alopecia* (b/c hair breaks off/ bald spots form), and *Keratomycosis (diseased cornea)* (can move from hair to cornea) can also occur. *Tinea favosa is a form of Tinea capitis (caused by Trichophyton schoenleinii) (favorite place to infect is the cap of the head, specifically on man Lenny- picture of lenny with cap and bald spot)*. -occurs when mycelia interact with scalp proteins producing *dead cell masses* in mats of hair and then develop into *yellowish-brown, cup-shaped skin crusts* (Lenny balancing cup on top of head) (scutula) with loss of hair and scarring. Diagnosis: -Chains of *macroconidia* (Macro- large piece of macaroni) and hyphae are seen on stained hair shafts. Treatment: *Griseofulvin* is used for treatment. (grizzly bear in picture) (Most infections resolve rapidly and spontaneously).

Superficial Mycoses: Black piedra

Cause: -*Piedra hortae* (horton the elephant is black/gray) is a black monomorphic mold that produces a *superficial mycosis of hair shafts* (pee from genitals w/ hair). Epidemiology: Piedra hortae is found in *South America* (tropical areas TQ TQ) as normal human flora, in *soil or animals* (Transmission is by person-to-person, non-human mammal-to-person contact or by contact with contaminated fomites). Pathogenesis: The *incubation period is days* (medium) -Infection of hairs of the scalp forms *mycelial and nodular swellings* along the axis of hair shafts causing the *hair to weaken and break off* (loose hair TQ TQ, in white pedria just get dandruff) due to keratinolytic activity. -Partial or protective immunity do not follow infection (can get piedra/dandruff over and over again). Symptoms: *Gritty, hard black encrustations* of cemented hyphal cells form *painless nodules* (dandriff doesn't hurt) on hair shafts of the *head* (dandriff can be on genitals) . -It looks like *black dandruff* Diagnosis: Staining of cross sections of hairs show hair shafts with black, hard gritty nodules containing *asci with multiple ascospores* -(can even happen on ass hairs) Treatment: *Selenium sulfide* (head and shoulders) is used for treatment.

Tinea barbae

Cause: -*Trichophyton* (faces can be three color - Tri- colors) species are monomorphic molds that cause cutaneous mycoses of *hairy areas of the skin* - main difference from tinea facei (face and neck). Epidemiology: Fungal species are *found worldwide* (same as facei) in humans and non-human mammals (reservoirs- same as facei). (It is transmitted by person-to-person, by contaminated fomites, by non-human mammals-to-people or by aerial dissemination and is communicable as long as infective lesions are present)- *same as facei*. Pathogenesis: The incubation period is *days to weeks* - same as facei Mycelia grow into pores around hair shafts, beneath the cuticle of hairs or *in the stratum corneum layer* (b/c tinea) of the skin. Hyphae growing into the stratum corneum produce *edema and leukocytic infiltrations* (same as facei) -> faC/KE enzymes -> attract lymphocytes -Partial protective immunity follows infection (man with PPI hat and rash on face- same as facei). Symptoms: The mild superficial type is characterized by *scaling lesions with a vesiculopustular border* (same as facei) on the bearded areas of the face and neck (main difference from facei is HAIR infection) The deep pustular type has deep, follicular pustules on the bearded areas of the face and neck that result in: -*nodular keloids (dry lesions) and kerions (wet lesions) with alopecia (loss of hair)* and scarring. (keloid = overgrowth of scar tissue). (man with face rash and K sticker) Diagnosis: Stained preparations of lesion scrapings or diseased hair show different types of *microconidia* (micro macaroni in picture) - same as facei on hyphae, depending on the fungal species. Treatment: *Griseofulvin* - hairy grizzly bear- (halts mitosis)

Tinea faciei

Cause: -*Trichophyton* (faces can be three color - Tri- colors) species are monomorphic molds that cause cutaneous mycoses of the *glabrous (smooth) skin of the face* Epidemiology: -Infectious agents are *found worldwide* (everywhere can get face rashes) on *humans and non- human mammal reservoirs* (can get from another person) -transmitted from person-to-person, by *aerial dissemination* (can get from just being close to someone else), on fomites or non-human mammals-to-people. Patients are usually *10 to 40 years of age* (large range, not in kids, not in elderly). Pathogenesis: The *incubation period is days to weeks* (longer than ones before, takes longer to accumulate on face). -*Hyphae growing into the stratum corneum* (b/c tinea species) produce *edema and leukocytic infiltrations by releasing collagenase, keratinase and elastase* (faC/KE) enzymes that destroy skin proteins. -(*Mold allergins cause granuloma formations. This occurs with all of the following dermatophyte (face) infections*). -Mycelia invade the glabrous skin of the face including the chin and upper lip of children and females but *excluding the mustache and bearded areas of the adult male* TQ (only glabarous skin) *Partial protective immunity develops following infection* (PPI hat on man with face rash) Symptoms: *Scaling, annular/circular lesions with raised margins and papules* are formed. (*sacled and circular* TQ) -Pruritus, burning and erythema are present. Diagnosis: -Stained preparations show hyphae with *microconidia* (micro/small piece of macaroni) (more common so far than macro) Treatment: *Miconazole* (ole = steroid inhibition) is used for treatment.

White piedra

Cause: -*Trichosporon ovoides* (of tricholors this one is void of color -> white) is a *white monomorphic mold* that causes a superficial mycosis of hair shafts. Epidemiology: The mold, Trichosporon ovoides, is *found worldwide* (black piedra only in tropical environment, dandruff you can get anywhere) in stagnant *water and soil*, as normal flora of humans and non-human mammals. (It is transmitted by person-to-person or mammal-to-person contact or by contact with contaminated fomites) Pathogenesis: The *incubation period is days* (medium). Infection of the hair results in *white, mycelial and nodular swellings* along the axis of hair shafts, *weakening and breaking them off*. -(Partial or protective immunity do not follow infection)- can get dandriff many times Symptoms: -Soft, white, painless nodules form around the cuticle of hair shafts resulting in crusts on the skin or hair of the *head or genitals* -The color of the lesions is produced by the white fungus. Diagnosis: -Staining of skin scrapings show hair shafts containing *conidia* (white cones) with white nodules and *hyaline* (hyaline = clear), septate hyphae that are broken up into arthrospores (spread so easily to rest of head b/c of spores). Treatment: *Selenium sulfide* is used for therapy.

Chemotherapy for fungi

Chemotherapy for fungi: *Flucytosine* -(enters fungal cells and is) *deaminated to fluorouracil* that *represses pyrimidine metabolism* (flucy to flouro- represses DNA building) *Griseofulvin* -*inhibits mitosis at metaphase* by interaction with *microtubules* (resulting in disruption of mitotic spindles) and also *binds to intracellular lipids* resulting in stunting and *shrinking hyphae* (griz, scares mitosis) *Pentamidine isethionate* -interferes with nuclear functions and metabolism by *inhibition of DNA synthesis* (pentamine -> dna synthesis) Compounds that change membrane permeability: *Amphotericin B* and *nystatin* -*deplete ergosterol* (and do not allow it to be incorporated into fungal cytoplasmic membranes). (amphibian and stat -> steroid) *Fluconazole, ketoconazole, miconazole, thiabendazole etc. ( imidazoles)* ('ole' drugs). -*inhibit ergosterol synthesis* by preventing *conversion of lanosterol to ergosterol* (in the cytoplasmic membrane resulting in loss of cell membrane integrity). ("ole" drugs = swole drugs= steroids) *Terbinafine's* -fungicidal toxicity is due to its role in the toxic *accumulation of squalene* that *depletes ergosterol* in the cell membrane. (turbo = snail = steroids)

Myiasis

Dr Mayi Cause: *Cochiomyia (dr mayi drinking coco)* species are new world *screwworm flies (worm in spiral)*, *Dermatobia species are human bot flies (skin is roobot metal)*, *Cuterebra species are warble flies (cute bra)* and *Cordylobia species are Mango flies (mango connected by cord)*, all are insects. Epidemiology: Myiasis producing flies are found worldwide and have humans and non-human mammals as reservoirs and intermediate hosts. Life Cycle: Adult flies lay eggs on human skin, eggs hatch into larvae that invade healthy or necrotic tissue and then become pupae and fall to the ground to further develop into adult flies (*complete metamorphosis (baby into full adult)* Adult flies *do not infest or suck blood from humans (red straw with X through it)* Pathogenesis: The incubation period is hours to days. The location of the larvae determines the significance of its presence. Fly larvae secrete lytic enzymes that allow them to penetrate tissues and live in humans. Ingested fly eggs on food produce *intestinal lesions and maggots (army general for maggots)* on the skin cause necrotic, pus-filled lesions. Adult flies are intermediate hosts and vectors of parasitic diseases. Partial or protective immunity do not follow infestation. Symptoms: Myiasis presents with swollen, fairly *painless lesions (smile)* that are *self-healing (patient is also doctor)* after the larvae pupates and falls out of a skin lesion. If disturbed by scratching, tissue damage can result in considerable pain. If female flies lay their eggs in the nostrils of sleeping humans, dozens of maggots migrate throughout the *mucous membranes and sinuses* (draw sinuses on patient)* *Ocular, intraocular and orbital opthalmomyiasis (draw red around eyes)* and urogenital, rectal or intestinal forms can occur. Diagnosis: Diagnosis is by a history of contact with the insect or by identification of larvae. Treatment: Larvae are removed *surgically* after a 48 hour application of vaseline and irrigation of the wound prevents bacterial infections. Good sanitation prevents infestations, either skin or food borne types.

Dirofilariasis

Fills the heart (normally the heart fills the body) Cause: -*Dirofilaria immitis* is the arthropod-borne *dog heartworm (dog with worm coming from heart)* Epidemiology: Dirofilaria immitis is found worldwide and has dogs and sometimes other non-human mammals as reservoirs. Life Cycle: Adult worms live in the *hearts of dogs (definitive hosts)* *Microfilariae (mini gas pumps- for filling)* are released into the bloodstream, nocturnally, where they are picked up by mosquitoes during a blood meal (Aedes and Culex species). Following development in the *mosquito (intermediate host and vector) (draw picture of mosquitto biting dogs)*, microfilariae are injected into dogs or humans during a blood meal. In dogs, the larvae develop into adult worms in the heart and pulmonary artery. In humans (accidental hosts), the larvae stay in the subcutaneous tissues or *migrate to the lungs (draw lungs for human patient*) but do not completely develop into adult worms. Pathogenesis: The incubation period in humans is hours to days for larval lesions and months for adult worm formation. Microfilariae are trapped in skin or lung tissues following *injection by mosquitoes* and produce allergic reactions resulting in subcutaneous nodules and *infarcts (patient farting)*, abscesses or encapsulated pulmonary nodules or tumors. Partial or protective immunity do not follow infection. Symptoms: *Coin-shaped lesions (coin on patient)* develop in the skin producing solitary, peripheral nodules or in the lungs producing coughing, chest pain, eosinophilia, *hemoptysis (patient coughing up blood)* and fever. Adult worms in human hearts have been reported but microfilariae were not found in the blood. Diagnosis: Diagnosis is by clinical symptoms, by locating coin lesions, by x-rays, by a history of exposure, or by finding larvae in tissues. Treatment: *Surgical removal (knife and surgery mask)* of larvae is used for therapy.

Fungi

Fungi can be either: 1) single cells called yeasts (yeasts yern b/c alone) 2) multicellular filamentous colonies called molds (molds = multicellular) -can be *monomorphic: occur as yeast or mold but not both* -can be *dimorphic and grow as yeast and mold forms: grow as yeast at body temperature and as molds at room temperature.* (yeasts, alone, nobody survives with them) -identified by: 1) *asexual spore morphology* 2) *spore formation* 3) *structure of (spore-bearing) mycelium* -(branching, thread like hyphae)

Fungus pathogenicity

Fungus pathogenicity: Fungi are *chemoheterotrophic* because they obtain carbon compounds from nonliving organic material as *saprophytes* or living tissues as *symbionts* -Pathogenic symbionts are either necrotrophic or biotrophic parasites: *Necrotrophic* fungi are *facultative pathogens* that live on damaged tissue and usually bring about the death of their hosts. *Biotrophic* fungi are *obligate pathogens*, dependent on living host tissues. Virulence: -(Fungi secrete a variety of enzymes (proteases, elastases and phospholipases) that are virulence factors because they cause host cell damage and lysis and impair antifungal host defenses) -*Toxins* act as *allergens and cause granulomas.* -*Mannan*, a glycoprotein component of fungal cell walls, *suppresses lymphoblast formation*. *Also inhibits keratinocyte proliferation*- *slowing epidermal turnover* (mannan- men don't need skin or WBC's!). -Cultures with: 1) *normal growth rate are virulent* 2) *lower growth rates (lacking invasive enzymes) are avirulent* - growth rate is a determinant of virulence. (grow slow, not dangerous).

Linuche unguiculata - Sea lice envenomization

Lynch the jellyfish Cause: *Linuche unguiculata is a thimble jellyfish (jellyfish in shape of thumb)*, a *coelenterate (living in a co-op)*. Epidemiology: Linuche unguiculata is found along *South Florida's coastline (south florida only on map)* from mid-May through early July and is a *free-living, ocean-dwelling jellyfish (draw ocean)*, feeding on small aquatic crustaceans. Life Cycle: *Microscopic larvae (microscope)* of Linuche unguiculata are intermediate forms in the development of the thimble jellyfish (no larger than a thumb-tip) that float freely in the ocean. Easterly winds blow the jellyfish to the shoreline where the *invisible, microscopic larvae (plankton-size) are released into the sea when the jellyfish spawn* Pathogenesis: The stings are felt immediately upon contact or lesions can develop days later. Swimmers are stung when sea lice become trapped and squeezed under their bathing suits. One in every four swimmers are stung whenever sea lice are present in the ocean. Different people have different reactions to the stings of the larvae, from a mild skin irritation to severe allergic responses and anaphylaxis Partial or protective immunity do not follow exposure. Symptoms: Itchy, red skin reactions develop into hives and swellings that can persist for up to two weeks. Allergic reactions due to being stung on multiple occasions can result in *difficulty in breathing (ventilator)* Diagnosis: Diagnosis is by a history of swimming in the ocean along with the presence of painful cutaneous lesions. Treatment: *Antihistamines and antivenin* (snake with venom and hissing)* are used for therapy

Cutaneous larva migrans (Creeping eruption)

Migrating larvae (worms) -> move to ankle Cause: -*Ancylostoma braziliense and Ancylostoma caninum (dogs in Brazil) are *non- arthropod-borne dog and cat hookworms (X through mosquitto, draw dog and cat). Epidemiology: Ancylostoma braziliense and Ancylostoma caninum are found worldwide and have dogs and cats as reservoirs. Life Cycles: Adult worms live in the *small intestines (draw S.I on dog and cat)* of dogs and cats (definitive hosts) and eggs pass out with *feces (draw feces)* Larvae hatch out of eggs and develop into *filariform larvae (poop with flour)* on vegetation and on moist soil. Humans are dead-end hosts when the infective larvae accidentally penetrate the skin on contact (they think you are a dog or cat). Pathogenesis: The incubation period is days. Larvae penetrate the skin and wander around under the dermis of humans but never enter the blood stream, thus producing an inflammation of the epidermis. Local *eosinophilia (big E on ankle)* occurs around the tunnels and lesions persist for months if untreated. Partial or protective immunity do not follow infection. Symptoms: Patients develop symptoms a few hours after larval penetration of the skin. *Serpiginous tunnels (draw snake in tunnel)* form in the epidermis causing pruritic, reddish papules with *edema (E for edema)*. The tunnel tracks can advance *several centimeters in one day (ruler)* Hypersensitive individuals develop vesicles and bullae at the site of entry. Tunnels become dry and crusted. Diagnosis: Diagnosis is by clinical symptoms, a history of exposure or rarely finding larvae in a tissue biopsy from the leading edge of a serpiginous track. Treatment: *Albendazole (person bending over)* is used for treatment. If untreated, the larvae will die in several months and the symptoms will go away.

Trombidiosis

Mike trumbo (the baseball player) Cause: -*Eutrombicula alfreddugesi (talking to alfred from batman)* (chigger mite, red bugs) is an *arachnid (draw spider)* Epidemiology: Eutrombicula alfreddugesi is found worldwide and has *domestic and wild animals, birds (draw birds)* and humans as intermediate hosts. Transmission is by contact with *tall weeds (draw long grass)* and grass containing mites that crawl up the legs and *attach to the skin by the capitulum* Life Cycle: Adult mites are *free-living herbivores (like grass)* and predators found in grassy or bushy terrain frequented by domesticated animals, wild rodents or birds. *Eggs are laid in clusters (show cluster of eggs)* on moist ground rich in humus, hatch and larval mites hatch and are *ectoparasites (draw red outside of hairs)* on humans usually falling off before they are seen and become nymphs and finally, adult mites. The life cycle is 50 to 70 days and the adult females live over a year. Pathogenesis: The incubation period is hours to days. Lesions occur when mite larvae bite through the skin of humans injecting *saliva that is antigenic and contains lytic compounds (draw saliva coming from bug mouth)* that dissolve tissue that is then used as food by the mites. *Larvae do not suck blood* or burrow into the skin. Necrotic reactions and *allergic reactions develop following a FIRST exposure (pack of benadryl)* Partial or protective immunity do not follow infestation. Symptoms: Small, itching red spots develop into a dermatitis consisting of pustules and *wheals (draw a few wheels)* beginning around the ankles, knees, waist, wrists and in other places where clothing is tight, usually on the second day. Deep red lesions with attendant *loss of sleep (patient with bags under eyes)* may last for days to weeks when the swelling finally subsides. Severe infestations may produce fever and bacterial infections occur due to scratching. Diagnosis: Diagnosis is by history of the bite, by capture and identification of the arthropod and by clinical symptoms. Treatment: *Steroids* are used as therapy.

Types of organism relationships

Normal flora: -organisms that are *normally and consistently* found in or on the body in the *absence of disease*. Symbiosis: -the close association or *living together* of organisms of different species. 1) Commensalism -type of symbiosis where a *parasite is benefited* and the *host is neither benefited nor harmed* by the relationship. 2) Mutualism -type of symbiosis in which *both host and parasite benefit* (the benefit is mutual) Parasitism -an obligatory relationship in which *one organism, is metabolically dependent on another.* *The host is usually harmed* TQ TQ big differentiator

Trematodes Schistosome dermatitis (Swimmer's itch)

Patient with schitzofrenia (seeing crazy things, clowns) Cause: -Schistosoma species are *trematodes (draw toad/frog)* that have non-human animals or birds as hosts and are infectious for humans. Epidemiology: Schistosoma species are found worldwide in *fresh or salt water (draw waves for salt water)* and have *animals or birds as reservoirs and definitive hosts (show bird giving disease to patient)* Life Cycle: Adult worms live in the *blood vessels (draw heart and vasculature*) of animals and birds and release eggs that migrate to the *digestive tract, pass out with feces (draw patient feces)* Miracidia hatch, penetrate *snails (draw snails)* (intermediate hosts) and develop into *cercaria (snails really care about patient, draw smooches)* that are released in water. Cercaria can accidentally penetrate the skin of humans (dead-end hosts) when contact is made in fresh or saltwater. Pathogenesis: The incubation period is hours to days. Cercaria migrate under the skin of humans producing mechanical and *toxic damage (skull for toxic)* but do not enter blood vessels and become adults. Foreign proteins from the cercaria induce inflammatory responses in human skin tissue producing *serpiginous tunnels (snake in tunnel*) where the cercaria eventually die. Delayed hypersensitivity to the cercaria can develop following re-exposure. Partial or protective immunity do not follow infection. Symptoms: -*Tunnel lesions* are produced and result in vesicles, papules, *hemorrhagic rash and pustules with itching (water bottle spilling over -hemmorhage)* and secondary bacterial infections in humans. Lesions from primary infections go away after 4 to 5 days but persist when hypersensitivity is present. Diagnosis: Diagnosis is by observation of clinical symptoms, history of exposure and the finding of *larvae (lard -> very fat patient)* in tissue biopsies. Treatment: *Antihistamines (snake hissing)* are used for therapy. Prevention is by use of repellents or by skin covering creams.

Phylum Protozoa -Protozoans- One-celled Organisms

Phylum *Protozoa (pros)* 1.Microscopic, *unicellular (#1 players in the world)* organisms, (ranging in size from one micron (Subphylum Microsporidia) to 100 microns (the other three subphyla)). 2. Locomotion is by *flagella and undulating membranes (*basketball players shown with flagella to help them jump higher)(underhand dunk)* (undulating membrane is extension of flagella into cell). (Subphylum Mastigophora), *cilia (SIA performing)* (Subphylum Ciliophora), or *pseudopodia (Sue bird)* (Subphylum Sarcodina). 3. *Outer cell membrane* also controls *fluid and food uptake (taking in food and fluids as they play* 4. *Interior protoplasm is differentiated into a nucleus, cytoplasm and organelles (t-shirts (interior) have N.O.C)* 4.a. *Cytoplasm* consists of a *thin outer ectoplasm* and a *large inner endoplasm (spasm -> referee going crazy)* -mitochondria and stored food vacuoles. (ectoplasm outside, endoplasm inside) 4.b. *Nucleus* contains an outer nuclear membrane and an *inner reticulum - chromatin and a karyosome (louis CK watching)*

Phylum Nematoda - Nematodes - Round Worms

Phylum Nematoda - *Nematodes* - *Round Worms* (Neema -> traveling a-round the world)* 1.Adult worms are elongate cylindrical worms ranging from 1 to 30 centimeters in length. *lengths: protozoan< flatworm < roundworm < tapeworm* 2. The adult worm's *outer body wall is stiff* and has a *clear, non-cellular cuticle (wearing clear glasses)* with a subcuticular epithelium and a *layer of muscle cells (neema with bid muscles)* for movement. 2.a. The adult worm buccal cavity contains *hooks, teeth, lips or plates (show large teeth and holding a plate)* used for tissue abrasion or attachment. 3. Adult worms have a well-developed digestive system and *feed by sucking host blood (red straw sucking blood)* or *ingesting lysed tissues or intestinal contents* (round worms are vampires). 3.a. The *alimentary tract* is an *elongated tube (draw string from mouth to anus)* consisting of an (oral cavity, esophagus, midgut, hindgut and an anus) 4. Larval worms undergo *molting (draw volcano -> molting lava* in order to increase their body size during their growth phase of the life cycle usually existing in *host tissues or organs* 5. Nematodes are *dioecious (draw man with ONLY penis)* (with male and female reproductive organs found in different organisms (separate sexes)).

Phylum Platyhelminthes - Flat Worms: Class Trematoda -Trematodes- Flukes

Platy-helminths: *Flat worms*- trematoda* and flukes: (centered around Flat girls, trees and toads 1.Adult worms range from 1 to 5 centimeters in length and are *flattened (leaf-like)* TQ (*schistosomes are cylindrical*). 2. Adult worms body *wall is a non-cellular integument* containing *mitochondria and vacuoles* and is covered with *spines or tubercles (draw females with exaggerated spines)* 2.a. The *adults* contains *muscular suckers (sucking blood from boys)* and/or *spines or hooklets (girls with hooks for hands)* located anteriorly and ventrally that are used for *attachment* to the host. (adults are suckers) (great at attaching) 3. Adult worms *do not have a body cavity* but have a digestive tract that consists of a *muscular pharynx that bifurcates to form two posterior tubes (draw road that bifurcates into two)* 4. The worms life cycle always includes a *snail intermediate host (draw snails on top of toad looking at tree)* 4.a. Adult worm releases *eggs* when mature, *into the body cavities of their host* (so into snails). 5. The trematode productive system consists of *ovaries and testes present in each individual* (hermaphroditic) that allows *self-fertilization (draw girls with penis and vagina)*

Protozoa therapy

Protozoas: Antimony sodium gluconate: -*blocks energy production* in protozoan cells. (gluconate- eats up glucose) Chloroquine: -*inhibits hemoglobin breakdown* in human erythrocytes. (chlorine makes blood clean- no hemolysis) Metronidazole and diloxanide furoate -bind to and *inhibit DNA synthesis and protein formation* in protozoans. (no metro, you're furious, you can't make anything (trips)). Nifurtimox: -produces high levels of hydrogen peroxide that *inhibits DNA synthesis* and damages protozoan cell membranes. (no fur -> can't make anything (jackets). Paromomycin: -*binds to ribosomal RNA* causing defective polypeptide chains to be produced. (para- next to DNA = RNA) Propamidine: -produces *mitochondrial membrane damage* in protozoan cells. (proper energy/ propel is from mitochondria). Pyrimethamine sulfadiazine and trimethoprim sulfamethoxazole: -*inhibit DNA synthesis AND disrupt mitochondria* in protozoa. (meth = messes up BOTH life (DNA) and energy (mitochondria) Suramin: -inhibits enzyme activity and *damages intracellular organelles* of protozoa. (sure way to kill cell is to damage organelles)

Scabies

Rabies-show dog Cause: *Sarcoptes scabiei (sciclops dog)* (mange mite) is an *arachnid (draw spider)* Epidemiology: Sarcoptes scabiei is found worldwide and has *humans and dogs* as reservoirs and definitive hosts. Infection is most common in slum sections, *jails (dog in jail)* and armies. Transmission is by *intimate (sex clubs sign)* human-to-human contact. Life Cycle: Adult males and females mate on the outside of the skin and then penetrate the skin. Males excavate *pockets (dog with pockets)* or branches in the burrows. Adult female mites, activated by warmth, lay eggs in *tunnels (draw tunnel nearby)* they have produced in the skin. Larval forms hatch in days and leave the tunnels to infect new hosts or to re-infect new burrows in the same host. Females survive off the host for days. Pathogenesis: Mites live in *serpiginous, cutaneous burrows (snake in tunnel)* in humans and progress *without symptoms (large A for asymptomatic)* before being noticed. Multiple papular, vesicular or pustular lesions are produced by *allergic reactions (benadryl packet)* to eggs, larvae, adult mites or to mite excrement. Partial or protective immunity do not follow infestation. Symptoms: Patients have reddish, *elevated tracts (draw an elevator)* in the skin between the fingers, wrists and forearms, the bend of the knee and elbow, the inguinal area, penis and the shoulder blades that develop into single lesions or rash-like lesions occurring in tracks. Intense itching leads to scratching that spreads the infection, irritates the lesions and induces secondary bacterial infections. Lesions can develop into erythematous eruptions and granulomas due to *hypersensitivity*. The disease is referred to as the *"seven year itch." (large 7)* Diagnosis: Staining of follicle or skin scrapings show round mites with *short legs TQ- dogs have short legs in picture)* Chronic cases have fewer mites. Treatment: *Permethrin (draw meth rocks)* is used for therapy. Hot soapy baths can help.

Replication of fungi

Replication of fungi: -grow as *saprophytes* - *on living or dead organisms.* -are *heterotrophs (incapable of producing their own energy)* that are *saprophytes- decomposing dead material* (using it as food). -*excrete extracellular enzymes* - digest food outside of the fungal cells. -(habitats including air, water, soil, plants and animals). -will grow on *Sabourauds Dextrose* Agar at 25 or 37 degrees C. -growth may require 4 to 6 weeks. -growth is aided by the presence of antibiotics. -primarily *disseminate by ASEXUAL spores* -Fungi reproduce asexually by *budding* (the unequal division of one cell into two cells), by *fragmentation (pieces of hyphae grow)* or by *spore formation* (haploid cells) followed by dispersal. -Asexual sporulation of yeasts occurs when a process called *budding produces blastospores*. -*Long chains of elongated yeast* cells are called *pseudohyphae* The pathogenic fungi are able to grow indefinitely as *saprophytes* and are *not dependent upon mammalian or avian hosts*

Laboratory diagnosis of fungi

Stains: *Potassium hydroxide (KOH)* -is used as a *quick and inexpensive* way of viewing clinical specimens for the presence of fungal elements. -*causes most human tissue elements to become dissolved* leaving fungal elements such as conidia or hyphae that *retain their shape and color* and can be seen with *light microscopy* *Periodic Acid-Schiff (PAS)* -used to stain *polysaccharides* found in the *cell walls* of molds and yeasts. -has *aldehyde groups* that bind to *basic fuchsin* and stain the fungal elements *red* (acid schiff - an acid looking for basic groups- acidic so turns the element red). *Giemsa stain* -used when *intracellular structures* are to be examined. -stains tissue and blood cells showing *blue-colored* intracellular yeasts, sometimes with a *halo* around them. (Gems are found inside treasure chests- blue b/c can't breathe. Large halo on top of treasure chest to signal look here). *Nigrosin stain* -used to demonstrate *capsules around cells* (negros chained and can't move = capsule).

Laboratory Diagnosis of parasites

The following are six methods of identifying parasite life stages in either feces, blood or tissue exudates. 1) Fecal concentrations -used to concentrate parasitic forms in fecal samples. -based on the fact that *parasitic forms will float in zinc sulfate* TQ solutions of high osmolarity (specimens can be collected onto a glass slide and observed with a light microscope). 2) Trichrome stain -a standard procedure used for *staining parasites in fecal material* -stains protozoan cells *pink with blue-green organelles* (tri chome= three colors- pink, blue and green). 3) Acid-fast stain is used to find and identify *small protozoans in fecal smears* -stains cells *pink with a blue background* making them easy to find. (acid= red/pink) (blue background to contrast red/pink). 4) KOH preparations -quick and inexpensive way of viewing clinical specimens for the presence of *microscopic arthropods* -cause *most tissue elements to become dissolved leaving parasitic forms* (review from earlier) that retain their shape and color and are observed with light microscopy. 5) Giemsa stain -used when *intracellular* TQ structures are to be examined. -stains tissue and blood cells showing *blue-colored intracellular parasites, sometimes with a halo around them* (review from before- treasure chest gems). 6) Wright's stain -for identification of cell types in *blood smears*. -stains leucocytes and erythrocytes as well as protozoans or microfilariae in blood smears. (right to give blood).

Trematodes, Cestodes, Nematodes, Arthropod therapy

Trematoda Praziquantel: -*increases calcium permeability* producing a muscle paralysis and vacuolization and vesiculation of a trematode worm's tegument. (also used for cestodes) (do the quan- dab is a freeze movement - muscle paralysis Cestoda Niclosamide: -*uncouples oxidative phosphorylation* in tapeworm mitochondria. (close to mitochondria core is cortex- where os phox happens). Nematoda Diethylcarbamazine: -*damages microfilarial membranes* and immobilizes nematode larvae. (magazine -> needs transporters to be delivered -> microfilaments) Albendazole, Mebendazole, Thiabendazole and Triclabendazole ("bendazole drugs") -bind to nematode tubulin and *inhibits cytoplasmic microtubule formation* in nematode cells *stopping cell division* (bends the cell cycle circle -> halts it). Ivermectin: -increases chloride permeability producing a paralysis of nematode muscles. (iverson = cleans the scoreboard (chlorine = cleaning) Arthropoda Malathion: -is a neurological poison for arthropods that *overstimulates the nicotinic acetylcholine receptors* in the nervous system resulting in muscle rigidity, weakness and paralysis. (marathon running -> get high parasympathetics after while resting (acetylcholine)). Permethrins: -are *neurotoxins* that damage neuron membranes by *prolonging sodium channel activation* -(promethius -> poision to sodium channels).

Trichomoniasis

Tri-moans - three moans Cause: -*Trichomonas vaginalis* is a *non-arthropod (mosquitto with X)* -borne flagellated protozoan. Epidemiology: Trichomonas vaginalis is found worldwide and has humans only as reservoirs and definitive hosts. The infection is communicable for *months to years (365 calender)* in persistent infections. *Flagellated trophozoites (zoey with flagellas/tails*) (stage of protozoan life cycle) survive for 1 to 2 hours on moist surfaces and are viable for up to 24 hours in urine or semen. Life Cycle: Flagellated *trophozoites (zoeys) are transmitted by *sexual contact* or by droplets on contaminated fomites. They *live in the vagina (zoey has STD's)* and prostate of humans where they multiply and are passed directly to uninfected persons. A cyst stage is not present. Pathogenesis: The incubation period is days to weeks. Tissue damage is caused by the proliferation of colonies of *flagellated trophozoites* in the vagina or urinary tract. Flagellated trophozoites cause the destruction of epithelial cells producing leukocyte infiltration, inflammation, vaginitis and urethritis. No partial or protective immunity develops. Symptoms: Symptoms include vaginitis with *frothy, green or yellow vaginal secretions (froth- foamy from vagina)* associated with a foul odor and intense irritation. Severe cases in females are characterized by cervical hemorrhagic erosions, urethritis and with petechiae that can cause obstetric complications. Urethritis, prostatitis or sterility occurs in males but is usually asymptomatic persisting in the prostrate, urethra or seminal vesicles. Diagnosis: -*Pyriform (fire for pyro*), flagellated, motile trophozoites are found in vaginal or prostatic wet preparations. Treatment: *Metronidazole (classic drug for bacterial vaginitis)* is used for treatment. All sex partners must be treated. In the absence of treatment, self-cure results in 3 to 4 weeks.

Class Cestoda - Cestodes - Tapeworms

centered around a cess pool (fecees storage)- blocked off by tape Class Cestoda - *Cestodes* - *Tapeworms*: 1.Adult worms range from 1 to 60 centimeters in length, are *ribbon-like (draw ribbon on tape)* (segmented) and they *inhabit the intestinal tract (draw patient and their S.I)* of their hosts. 2. The body *wall is an enzyme active tegument (draw wall with big E on it)* containing *mitochondria, vacuoles, inclusion bodies and digestive enzymes* 2.a. Adult worms have a *scolex (draw rolex on patient)* (anterior attachment organ)) at one end with a *row of segments (proglottids) that originate from the head (show chain of strings attatched from the head)* forming a chain of segments (strobilum). 3. A *digestive tract is absent (big X over stomach area on WORM)* 4. *Larval forms are sac-like* containing developing tapeworm embryos and are found in host tissues and organs (flatworms use snails). 5. Proglottids are *hermaphroditic* (opposite of dioecious) containing a complete set of *male (testes) and female (ovaries) organs* allowing *self-fertilization (show patient which male and female genitals)* (each proglottids functions as an individual reproductive unit).

Visceral larva migrans

larvae migrate but more visceral- so in the eye Cause: -*Toxocara canis and Toxocara cati (draw dogs and cats again)* are non-arthropod-borne dog and cat roundworms. Epidemiology: Toxocara canis or Toxocara cati are found worldwide and have dogs and cats as reservoir and *definitive hosts (DS on dogs and cats)* (means parasites reproduce in them). Transmission is by the *fecal-oral (poop by mouth)* route from animals to humans, by eating *unwashed vegetables or dirt (draw stinky vegetables from the soil)*, or by eating raw infected *tissue of chickens, sheep or cattle (draw farm sign with cow)* (paratenic hosts). Life Cycles: Adult worms are only found in the *small intestines (draw SI on dogs and cats)* of dogs or cats (definitive hosts) and eggs are released with feces and develop on the ground. Eggs require 1 to 3 weeks incubation to be infective. When eggs are ingested by dogs or cats, infective larvae enter the bloodstream, *go to the lungs (draw lungs)* and then are coughed up and swallowed to become adult worms in the small intestine. Infected, pregnant female dogs pass the larvae through the placenta to the fetus and bare infected pups *(TORCH for dogs)* When humans (accidental hosts) ingest infective eggs, larvae enter the bloodstream and migrate extensively through visceral organs but *do not develop into adult worms (not definitive hosts)* Pathogenesis: The incubation period is weeks to months. Migrating larvae produce inflammation, *hypereosinophilia (big E for eosinophilia)*, skin rashes, fever, immune responses to polyprotein allergens and *granulomas (draw 1k $ sign in eyes)* in the eyes, lungs, kidneys and liver tissues. Damage depends on the number of eggs ingested, the migration routes of larvae in the tissues and the strength of immune response to the larvae. Partial or protective immunity do not follow infection. Symptoms: Fever, cough, pneumonitis, hepatomegaly, edema, *retinal granulomas and loss of vision* occur. Diagnosis: Diagnosis is by clinical symptoms, by a history of exposure or by finding larvae in tissue biopsies. Treatment: *Ivermectin (wearing allen iverson jersey)* and steroids are used for treatment.

Louse infestations

patient in louse -> "lice of louse" Cause: -*Pediculus humanus capitis is the head louse, Pediculus humanus corporis is the body louse and Phthirus pubis is the crab louse (draw young kids to show peeds)* All are *insects (draw caterpillar)* Epidemiology: *Lice (head itching)* are found worldwide and have *humans only as reservoirs and definitive hosts (animals crossed out)* Lice are transmitted person-to-person and by contact with fomites containing eggs or adults. Life Cycle: Lice undergo an *incomplete metamorphosis (draw half adult, have child)* but differ in their habits while infesting humans. Head lice stick eggs to hairs resulting in *visible nits (draw patient nitting)* Body lice lay their eggs in *clothing (draw person with full clothing)*. Crab lice lay eggs on hairs of the *eyebrows and pubic region (outline these regions)* Eggs hatch and develop into *nymphs (nymphomaniac- draw patient having sex)* that further develop into adults. Pathogenesis: Lice begin sucking blood as soon as they are on the body. Lice suck blood injecting saliva containing *lytic compounds (slice body = lysis)* that act as antigens resulting in *pustular (pust coming from body)* lesions at the site of the bite. Primary hypersensitivity to body lice is attained 3 to 8 months after the original infestation. *Lice serve as intermediate hosts* and vectors for viral, parasitic and bacterial diseases. Partial or protective immunity do not follow infestation. Symptoms: Patients have papules, ulcerations, anemia, intense itching and *discoloration (draw many colors)* at the site of bites. Scratching can result in excoriation and secondary bacterial infections. Toxic follicular conjunctivitis due to *hypersensitivity* (draw Hyper-sensitivty man- superhero)* to feces can occur. Diagnosis: Diagnosis is by a history of contact with the insects or simply by capture and identification of the insect. Treatment: *Malathion (draw track for marathon)* is used for treatment.

Dracunculiasis

the Dracula worm: Cause: Dracunculus medinensis is the *arthropod-borne guinea worm (picture of mosquitto with guinnea pig)* Epidemiology: Dracunculus mediensis is found in *Africa and Asia (map of Africa and Asia highlighted)* and has humans only as a reservoir and definitive host. Life Cycle: Adult worms live in the *connective tissue (CT on skin)* underneath the skin of humans. Larvae are released when the skin lesions come into contact with *water (water bottle)* Species of *Cyclops (patient has one eye)* (water flea; immediate host and vector) *ingest the larvae and the larvae develop into infective forms* When humans drink water containing the water fleas, larvae break out of the fleas, penetrate the mucosa of the stomach into the abdominal cavity, and migrate through the bloodstream to sites under the skin where they develop into adult worms. Pathogenesis: The incubation period is months. Adult worms release *metabolites (draw diet food*) into the connective tissue of humans that act as allergens and produce allergic reactions accompanied by an inflammatory response that results in *leukocytes surrounding the body of the worm creating resistance to its removal (draw WBC's around a worm)* Partial or protective immunity do not follow infection. Symptoms: Infections are asymptomatic during a year long incubation period. Symptoms include painful skin blisters, *urticaria (draw tic on body)*, nausea, vomiting, fever, myalgia and diarrhea. Ulcers become secondarily infected with bacteria that can result in serious complications. Infected patients are *incapacitated (patient holding barbell but can't lift it)* for several months once the skin ulcers occur. Diagnosis: Adult female worms are found extending from subcutaneous tissues releasing larvae into water. Treatment: *Steroids and topical antibiotics* are used to treat the infection. *Surgery* or physical removal of the worm by slowly wrapping it around a stick will shorten the duration of the infection. Patients should be given a *tetanus immunization (teta vaccine -> draw 4 vaccine syringes)* Control is by purification of the drinking water.

Loiasis

the low worm-> patient bending knees and low Cause: *Loa loa* is an arthropod-borne eye worm. Epidemiology: Loa loa is found in *Equatorial Africa (Africa on map)* and has humans only as reservoirs. Life Cycle: Adult worms of Loa loa live in the subcutaneous tissues of humans (definitive hosts) where they release *microfilariae into the bloodstream (show micro gas pumps or micro lab fillers- triangles) *Deer flies (draw deer)* (Chrysops species; intermediate hosts and vectors) living in *muddy streams and swamps* (draw black water and alligator)* pick up the microfilariae during a daytime blood meal. Microfilariae develop into infectious filariform larvae and are then transmitted to a new human host during another blood meal by leaving the *proboscis (draw dr boesler)* (means nose) and burrowing into the bite wound. Larvae migrate to the subcutaneous and *muscle tissues (draw big muscles)*, become encysted and develop into adult worms. Pathogenesis: The incubation period is months to years. Adult worms move around in the subcutaneous tissues releasing *metabolites (diet foods)* that produce an inflammatory reaction and an *eosinophilia (large E for eosinophilia)* Worms appear under the *conjunctiva of the eye (draw worms coming from eyes)* or under the skin and if not trapped and encapsulated, can disappear within minutes. Partial or protective immunity do not follow infection. Symptoms: Patients present with fever, *itching swellings (deet)* on the body, erythema, urticaria (tic on body)* due to the host's immune response, painless, subcutaneous Calabar swellings- TQ- (cal ripken jersey)* and renal or cardiac disease. Adult worms under the conjunctiva produce irritation, a *crawling sensation in the eye (draw worm with many legs)*, pain, congestion, periorbital swelling, *photophobia (draw holding sunglasses)*, interstitial keratitis and blindness. Diagnosis: The appearance of Calabar swellings, microfilariae found in stained blood smears or developing worms seen migrating under the conjunctivae or the skin are diagnostic. Treatment: *Diethylcarbamazine (carbohydrate magazine)* is used for treatment and as a prophylaxis for a select group of individuals.