Pharmaceutical Sciences Notes

NTA Level 5 • Semester 1 • PST05103 HIV and AIDS Pharmaceutical Microbiology • Source Session/Topic 30 Full source-text version: all educational wording from the extracted learning source is retained; only presenter/tutor metadata and web-layout noise are removed, while formatting is improved for readability. Session 30: HIV and AIDS Total Session Time: 60 minutes Pre-requisites • Human anatomy and physiology Students Learning Tasks By the end of this session students are expected to be able to: • Describe HIV and AIDS (causative agents, transmission, signs and symptoms) • Describe treatment, prevention and control of HIV and AIDS Resources Needed: • Flip charts, marker pens, and masking tape • Black/white board and chalk/whiteboard markers SESSION OVERVIEW |Step |Time |Activity/ |Content | | | |Method | | |1 |5 minutes |Presentation |Introduction, Learning Tasks | |2 | 15 minutes|Presentation |Cause and Transmission of HIV/AIDS| |3 |10 minutes |Buzzing/ |Signs and Symptoms of HIV/AIDS | | | |Presentation | | |4 | |Take home |Treatment, Prevention and Control | | |20 minutes |assignment/ |of HIV/AIDS | | | |Presentation | | |5 |5 minutes |Presentation |Key Points | | 6|5 minutes |Presentation |Evaluation | SESSION CONTENTS STEP 1: Presentation of Session Title and Learning Tasks (5 minutes) READ or ASK students to read the learning tasks and clarify ASK students if they have any questions before continuing STEP 2: Cause and Transmission of HIV/AIDS (15 minutes) • Human immunodeficiency virus (HIV) infection and acquired immune deficiency syndrome (AIDS) is a spectrum of conditions caused by infection with the human immunodeficiency virus. • HIV is a single-stranded positive-sense RNA virus that belongs to the family retroviridae. It infects HIV infects CD4-bearing cells (T4 lymphocytes and monocyte-macrophages) • HIV is transmitted through unprotected sexual intercourse with an infected person, blood to blood contact (e.g. using unsafe skin piercing instruments and blood transfusion), mother to child transmission during delivery and breastfeeding • Inside the host cell, HIV uses its own reverse transcriptase enzyme to produce DNA from its RNA genome, the reverse of the usual pattern • The new DNA is then incorporated into the host cell genome by an integrase enzyme to form viral DNA as part of its own genome, transcribing and translating the viral genes along with the cell's own genes, producing the proteins required to assemble new copies of the virus • It is difficult to detect the virus until it has infected the host. At that point, the infection will persist indefinitely • The Infection may be latent or chronic low level. • Activation leads to the development of immune dysfunction as a result of direct and indirect killing of T4 cells and functional impairment of viable T4 cells. • Macrophages appear to be the primary target cells in brain infection. The pathogenic mechanisms of neurologic disease are not known • A person can be infected with HIV but not have AIDS. • The virus infects human T-lymphocyte cells • Infection by the human immunodeficiency virus leads to gradual and progressive destruction of the cell mediated immune system. o Failure of the immune system allows life-threatening opportunistic infections and cancers to thrive STEP 3: Signs and Symptoms of HIV/AIDS (10 minutes) |Activity: Buzzing (5 minutes) | | | |ASK students to pair up and buzz on the following question for 2 | |minutes | | | |What are the signs and symptoms of HIV/AIDS? | | | |ALLOW few pairs to respond and let other pairs to add on points not | |mentioned | | | |WRITE their response on the flip chart/board | | | |CLARIFY and SUMMARIZE by using the content below | • HIV is associated with three presentations; o Asymptomatic infection o Acute infection with symptoms ▪ May include fever, sweats, myalgia or arthralgia, sore throat, lymphadenopathy, nausea, vomiting, diarrhea, persistent headaches, rash and generalized pruritus o Acquired immune deficiency syndrome (AIDS) ▪ Characterized by progressive immune deficiency accompanied by a wide range of opportunistic infections, neoplasms, and neurologic abnormalities, including progressive dementia and peripheral neuropathy. • Most patients, however, present with symptoms due to opportunistic infections e.g. tuberculosis, candidiasis or pyogenic infections. STEP 4: Treatment, Prevention and Control of HIV/AIDS (20 minutes) • Treatment of HIV/AIDS involves use of antiretroviral drugs • Classes of retroviral drugs used in Tanzania are; o Nucleotide/Nucleoside reverse transcriptase inhibitors (NRTIs) ▪ Zidovudine (AZT) ▪ Tenofovir (TDF) ▪ Abacavir (ABC) ▪ Lamivudine (3TC) ▪ Emtricitabine (FTC) ▪ Didanosine (DDI) o Non-nucleoside reverse transcriptase inhibitors (NNRTIs) ▪ Etravirine ▪ Efavirenz ▪ Nevirapine ▪ Etravirine ▪ Delavirdine o Protease inhibitors (Pls) ▪ Atazanavir ▪ Ritonavir (booster) ▪ Lopinavir ▪ Darunavir o Integrase strand transfer inhibitors (INSTI)/ Integrase inhibitors ▪ Dolutegravir (DTG) ▪ Raltegravir o Fusion inhibitors ▪ Enfuvirtide o Chemokine receptor inhibitors/CCR5 inhibitors ▪ Maraviroc |Activity: Take home Assignment (10 minutes) | | | |DIVIDE students in groups or individual. | | | |ASK the students to work on the following assignment | | | |What are the regimes (including drug name, dose and dose schedule) | |of antiretroviral drugs used; | |In treatment of adults and adolescents without tuberculosis | |In treatment of adults and adolescents with tuberculosis | |In pregnancy | |Drug abusers | |For post-exposure prophylaxis of medical staff | |For prevention of mother-to-child transmission | |In prophylaxis of babies born from infected mothers | | | |ALLOCATE time for students to do the assignment and submit | | | |REFER students to recommended references | • Prevention and control of HIV/AIDS o Safe sex practices e.g. use of condoms o Post exposure prophylaxis for people at risk e.g. medical staff o Prevention of mother-to-child transmission o Avoid sharing skin piercing instruments e.g. needles o Avoid drug abuse STEP 5: Key Points (5 minutes) • HIV is the virus that cause AIDS • A person may have HIV but not AIDS • AIDS occur when the body’s immune system is weakened by the virus so that the body cannot defend against infectious pathogens. • Treatment of HIV/AIDS involves the

NTA Level 5 • Semester 1 • PST05103 Introduction to Medical Mycology Pharmaceutical Microbiology • Source Session/Topic 31 Full source-text version: all educational wording from the extracted learning source is retained; only presenter/tutor metadata and web-layout noise are removed, while formatting is improved for readability. Session 31: Introduction to Medical Mycology Total Session Time: 120 minutes Pre-requisites • Human anatomy and physiology Students Learning Tasks By the end of this session students are expected to be able to: • Define common terms used in mycology • Describe occurrences and distributions of fungi • Describe the structure of a fungal cell • Classify fungi based on their sexual spores (zygomycota, Ascomycota, basidiomycotina, deuteromycota) Resources Needed: • Flip charts, marker pens, and masking tape • Black/white board and chalk/whiteboard markers • Hand out 35.1: Reproduction in Fungi SESSION OVERVIEW |Step |Time |Activity/ |Content | | | |Method | | |1 |5 minutes |Presentation |Introduction, Learning Tasks | |2 |20 minutes |Presentation |Common Terminologies used in | | | | |Mycology | |3 |10 minutes |Presentation |Occurrence and Distribution of | | | | |Fungi | |4 |15 minutes |Buzzing/ |Characteristics of Fungi | | | |Presentation | | |5 |25 minutes |Presentation |Fungal Growth and Reproduction | |6 |25 minutes |Presentation |Structure of Fungal Cells | |7 |10 minutes |Presentation |Classification of Fungi | |8 |5 minutes |Presentation |Key Points | |9 |5 minutes |Presentation |Evaluation | SESSION CONTENTS STEP 1: Presentation of Session Title and Learning Tasks (5 minutes) READ or ASK students to read the learning tasks and clarify ASK students if they have any questions before continuing STEP 2: Common Terminologies Used in Mycology (20 minutes) • Mycology o Mycology is the study of fungi • Mycosis o Mycosis is a term referring to infections caused by fungi • Mould o Hyphal or mycelial colony or form of growth • Mycelium o Mass or mat of hyphae, mould colony • Yeast o Unicellular, spherical to ellipsoid fungal cells that usually reproduce by budding • Budding o A common mode of asexual reproduction, typical of yeasts o During mitosis, the parent cell wall protrudes outwardly and enlarges to form a nascent bud that contains the progeny nucleus o A fungal cell may produce single or multiple buds • Spore o A specialized propagule with enhanced survival value, such as resistance to adverse conditions or structural features that promote dispersion. Spores may result from asexual (e.g. conidia, sporangiospores) or sexual reproduction • Dematiaceous fungi o Fungi whose cell walls contain melanin, which imparts a brown to black pigment • Dimorphic fungi o Fungi that have two growth forms, such as a mold and a yeast, which develop under different growth conditions (e.g. Blastomyces dermatitidis forms hyphae in vitro and yeasts in tissue) They are the cause of most fungal infection • Hyphae o Tubular, branching filaments of fungal cells, the mould form of growth. Septate hyphae are separated by porous cross-walls (or septa) and aseptate hyphae are continuous and also known as coenocitic hyphae. o o Vegetative or substrate hyphae anchor the colony and absorb nutrients o Aerial hyphae project above the colony and bear the reproductive structures • Pseudohyphae o Chains of elongated buds or blastoconidia; the septations between cells are constricted STEP 3: Occurrence and Distribution of Fungi (10 minutes) • Fungi represent one of the largest groups of living organisms and they play major roles in ecosystem processes • Fungi are among the most widely distributed organisms on Earth and are of great environmental and medical importance • Many fungi are free-living in soil or water; others form parasitic or symbiotic relationships with plants or animals • Fungi are distinguished from all other living organisms by their modes of vegetative growth and nutrient intake • Fungi grow from the tips of filaments (hyphae) that make up the bodies of the organisms (mycelia) and they digest organic matter externally before absorbing it into their mycelia • Fungi are either terrestrial or aquatic, the latter living in freshwater or marine environments • Freshwater species are usually found in clean, cool water because they do not tolerate high degrees of salinity • However, some species are found in slightly brackish water, and a few thrive in highly polluted streams • Soil that is rich in organic matter furnishes an ideal habitat for a large number of species; only a small number of species are found in drier areas or in habitats with little or no organic matter • Fungi are found in all temperate and tropical regions of the world where there is sufficient moisture to enable them to grow • A few species of fungi live in the Arctic and Antarctic regions, although they are rare and are more often found living in symbiosis with algae in the form of lichens STEP 4: Characteristics of Fungi (15 minutes) |Activity: Buzzing (5 minutes) | | | |ASK students to pair up and buzz on the following exercise for 2 | |minutes | | | |List the characteristics of fungi? | | | |ALLOW few pairs to respond and let other pairs to add on points not | |mentioned | | | |WRITE their response on the flip chart/board | | | |CLARIFY and SUMMARIZE by using the content below | • Fungi (yeast& molds) are eukaryotic organisms • Cell wall of fungi is made up of chitin o Chitin is a polysaccharide composed of long chain of N- acetyleglucasamine. o Also the fungal cell wall contains other polysaccharide, β-glucan • Fungi are heterotrophic in nutrition • They do not have chlorophyl • Reproduce by sexual and asexual methods • Most are multicellular (moulds) and some are unicellular (yeasts) STEP 5: Growth and Reproduction in Fungi (25 minutes) Fungal Growth • A typical fungus consists of a mass of branched, tubular filaments enclosed by a rigid cell wall made up a rigid polymer, chitin • The filaments, called hyphae (singular hypha), branch repeatedly into a complicated, radially expanding network called the

NTA Level 5 • Semester 1 • PST05103 Subcutaneous and Systemic Mycoses Pharmaceutical Microbiology • Source Session/Topic 32 Full source-text version: all educational wording from the extracted learning source is retained; only presenter/tutor metadata and web-layout noise are removed, while formatting is improved for readability. Session 32: Subcutaneous and Systemic Mycoses Total Session Time: 120 minutes Pre-requisites • Human anatomy and physiology Students Learning Tasks By the end of this session students are expected to be able to: • Classify and describe common mycoses (causative agents, transmission, signs and symptoms) • Describe treatment, prevention and control of common fungal diseases Resources Needed: • Flip charts, marker pens, and masking tape • Black/white board and chalk/whiteboard markers SESSION OVERVIEW |Step |Time |Activity/ |Content | | | |Method | | |1 |5 minutes |Presentation |Introduction, Learning Tasks | |2 |50 minutes |Presentation |Subcutaneous Mycoses | |3 |50 minutes |Presentation |Systemic Mycoses | |4 |10 minutes |Presentation |Key Points | | 5|5 minutes |Presentation |Evaluation | SESSION CONTENTS STEP 1: Presentation of Session Title and Learning Tasks (5 minutes) READ or ASK students to read the learning tasks and clarify ASK students if they have any questions before continuing STEP 2: Subcutaneous Mycoses (50 minutes) • The fungi that cause subcutaneous mycoses normally reside in soil or on vegetation. They enter the skin or subcutaneous tissue by traumatic inoculation with contaminated material. • Subcutaneous mycoses are less common than superficial fungal infections and are characterized by a heterogeneous group of infections that often result from direct penetration of the fungus into the dermis and subcutaneous tissue through traumatic injury • The fungus spreads by local deep tissue invasion from the inoculation site • The disease usually remains localized and then slowly spreads to adjacent tissue and eventually to the lymphatics • The common subcutaneous mycoses are sporotrichosis, chromoblastomycosis, phaeohyphomycosis, eumycotic mycetoma, and hyalohyphomycosis • Sporotrichosis o It is a chronic granulomatous infection caused by Sporothrix schenckii o The fungus is introduced into the skin by trauma o Present with facial lesions which becomes granulomatous o Draining lymphatics become thickened and cord-like o Multiple subcutaneous nodules and abscesses occur along the lymphatics o Treatment ▪ Oral Potassium iodide for weeks ▪ Oral antifungals e.g. itraconazole • Chromoblastomycosis o Chromoblastomycosis (chromomycosis) is a subcutaneous mycotic infection that is usually caused by traumatic inoculation of any of the recognized fungal agents, which reside in soil and vegetation o Caused by dematiaceous fungi (with melanized cell walls) Phialophora verrucosa, Fonsecaea pedrosoi, Fonsecaea compacta, Rhinocladiella aquaspersa, and Cladophialophora carrionii o The infection is chronic and characterized by the slow development of progressive granulomatous lesions that in time induce hyperplasia of the epidermal tissue o The fungi are introduced into the skin by trauma, often of the exposed legs or feet o Treatment involves ▪ Surgical excision with wide margins is the therapy of choice for small lesions. ▪ Antifungal agents e.g. flucytosine, itraconazole • Phaeohyphomycosis o Phaeohyphomycosis is a term applied to infections characterized by the presence of darkly pigmented septate hyphae in tissue o Signs and symptoms ▪ Cyst-Lump produced by over-secreting gland ▪ Skin lesions ▪ Skin infections ▪ Skin discoloration ▪ Pigmented lesions o Treatment ▪ Itraconazole ▪ Amphotericin B ▪ Oral phenytoin ▪ Voriconazole • Mycetoma o Mycetoma is a chronic subcutaneous infection induced by traumatic inoculation with any of several saprophytic species of fungi or actinomycetous bacteria that are normally found in soil o A “mycetoma” is a chronic granulomatous progressive inflammatory disease that involves the subcutaneous tissue after a traumatic inoculation of the causative organism o Mycetoma may be caused by fungi (Eumycetes) or by higher bacteria (actinomycetes) and therefore mycetoma are grouped into eumycetoma and actinomycetoma. o Presents with a painless subcutaneous mass which discharges to the skin surface o The lesion presents as a slowly progressive painless swelling at the site of previous trauma and gradually increase in size o It may spread to involve the skin and deep structures resulting in destruction of bone, deformity and loss of function with serious social and economic implications o Treatment ▪ Must establish cause (whether bacterial or fungal) ▪ Surgical ▪ Antibiotics for actinomycetoma (Amikacin, co-trimoxazole) • Drugs are usually combined ▪ Antifungals e.g. amphotericin B, itraconazole, miconazole and nystatin STEP 3: Systemic Mycosis (50 minutes) • These are fungal infections that affect internal organs, primarily involving the respiratory system normally occur by inhalation of spores which develop in the lungs. • The fungi are dimorphic • Majority are self-limiting and asymptomatic, while the rest are symptomatic and disseminate by haematogenous route • Systemic mycose are: o Blastomycosis ▪ Caused by inhalation of conidial spores of Blastomyces dematitidis ▪ Results in a chronic granulomatous infection ▪ Primary infection is pulmonary blastomycosis ▪ Secondary infection is caused by spreading to other organs including skin (cutaneous mycosis) ▪ Osteoarticular blastomycosis involves the spine, pelvis, cranial bones, ribs and long bones ▪ Treatment: Amphotericin B o Coccidioidomycosis ▪ Caused by inhalation of arthrospors of Coccidioides immitis ▪ Primary infection is in the lungs and secondary infection involves • Other organs of the body (skin, bone, joints and meninges) ▪ Treatment: Amphotericin B o Histoplasmosis ▪ This is fungal infection caused by inhalation of spore of Histoplasma capsulatum ▪ The disease affects the reticulo-endothelial system (RES), commonly in AIDS patients ▪ Treated by Amphotericin B o Paracoccidioidomycosis ▪ Caused by inhalation of spores of Paracoccidioides brasiliensis ▪ Primarily infects the lungs and sometimes gastrointestinal mucosa ▪ Starting from the primary sites, the fungi spread through blood or lymph into the skin, mucosa or lymphoid organs ▪ Treatment involves; • Areazole derivatives e.g. itraconazole • Amphotericin B • Sulphonamides STEP 4: Key Points (10 minutes) • Subcutaneous mycoses may be caused by dozens of environmental molds associated with vegetation and soil • These infections are usually acquired when minor cuts or scratches introduce soil or plant debris (e.g. splinters, thorns) containing the pathogenic fungus. • The ensuing infections are frequently chronic but rarely spread to deeper

NTA Level 5 • Semester 1 • PST05103 Superficial Mycoses Pharmaceutical Microbiology • Source Session/Topic 33 Full source-text version: all educational wording from the extracted learning source is retained; only presenter/tutor metadata and web-layout noise are removed, while formatting is improved for readability. Session 33: Superficial Mycoses Total Session Time: 60 minutes Pre-requisites • Human anatomy and physiology Students Learning Tasks By the end of this session students are expected to be able to: • Classify and describe Superficial mycoses (causative agents, transmission, signs and symptoms) • Describe treatment, prevention and control of superficial mycoses Resources Needed: • Flip charts, marker pens, and masking tape • Black/white board and chalk/whiteboard markers SESSION OVERVIEW |Step |Time |Activity/ |Content | | | |Method | | |1 |5 minutes |Presentation |Introduction, Learning Tasks | |2 | 45 minutes|Group |Features and Treatment of | | | |discussion/ |Superficial Mycoses | | | |Presentation | | |3 |5 minutes |Presentation |Key Points | | 4|5 minutes |Presentation |Evaluation | SESSION CONTENTS STEP 1: Presentation of Session Title and Learning Tasks (5 minutes) READ or ASK students to read the learning tasks and clarify ASK students if they have any questions before continuing STEP 2: Features and Treatment of Superficial Mycoses (45 minutes) • Superficial fungal infections arise from a pathogen that is restricted to the stratum corneum, with little or no tissue reaction • Important superficial mycoses are Tinea versicolor, Piedra and Tinea nigra • Tinea versicolor (Pityriasis versicolor) o It is a superficial chronic infection of stratum corneum o It is common worldwide and is caused by Malassezia spp, which are human saprophytes that sometimes switch from yeast to pathogenic mold forms o Three species of Malassezia are linked to tinea versicolor; ▪ Malassezia furfur ▪ Malassezia globose ▪ Malassezia sympodialis o Signs and symptoms are; ▪ Hyperpigmented or depigmented maculae on chest, back, arms and abdomen ▪ Does not illicit immune response, no discomfort ▪ Limited to the stratum corneum o Treatment ▪ Topical antifungal e.g. whitfield’s ointment, miconazole, itraconazole ▪ Oral azole • Piedra o (White and black piedra) is common in tropical regions of the world o White piedra is also endemic in temperate climates o Black piedra is caused by Piedraia hortae o White piedra is a superficial fungal infection of the hair shaft is caused by Trichosporon species e.g. Trichosporon beigelii o Signs and symptoms ▪ White piedra shows irregular, white, cream-colored, or brown soft nodules or gelatinous sheaths along the hair shaft ▪ They can be easily detached from the hair shaft ▪ White piedra is found in the hair of the beard, moustache, genitals, and axilla ▪ Eyebrow and eyelash involvement can also be present, while on the scalp, white piedra appears to be less common o Treatment involves shaving and application of topical antifungal agents e.g. terbinafine, and ketoconazole shampoo • Tinea nigra (Tinea nigra palmaris) o Is common in tropical areas o Is a superficial chronic and asymptomatic infection of the stratum corneum caused by the dematiaceous fungus Hortaea (Exophiala) werneckii o Lesions appear as a dark (brown to black) discoloration, often on the palm STEP 3: Key Points (5 minutes) • Superficial mycoses are among the most common of all communicable diseases • They are mainly caused by Malassezia species which presents as patches of hyper and hypopigmentation on skin • Piedra affects the hairy parts of the body STEP 5: Evaluation (5 minutes) • What is piedra? • How is Tinea nigra palmaris treated? References Hugo and Russell (2011), Pharmaceutical Microbiology 8th Edition, Willey- Blackwel publications Karen C. Carroll et al (2013); Jawetz, Melnick and Adelberg’s Medical Microbiology 26th Ed. McGraw Hill Co. Inc. Greenwood et al (2012); Medical Microbiology, 18th edition Churchill Livingstone Session 33: Superficial Mycoses Total Session Time: 60 minutes Pre-requisites • Human anatomy and physiology Students Learning Tasks By the end of this session students are expected to be able to: • Classify and describe Superficial mycoses (causative agents, transmission, signs and symptoms) • Describe treatment, prevention and control of superficial mycoses Resources Needed: • Flip charts, marker pens, and masking tape • Black/white board and chalk/whiteboard markers SESSION OVERVIEW |Step |Time |Activity/ |Content | | | |Method | | |1 |5 minutes |Presentation |Introduction, Learning Tasks | |2 | 45 minutes|Group |Features and Treatment of | | | |discussion/ |Superficial Mycoses | | | |Presentation | | |3 |5 minutes |Presentation |Key Points | | 4|5 minutes |Presentation |Evaluation | SESSION CONTENTS STEP 1: Presentation of Session Title and Learning Tasks (5 minutes) READ or ASK students to read the learning tasks and clarify ASK students if they have any questions before continuing STEP 2: Features and Treatment of Superficial Mycoses (45 minutes) • Superficial fungal infections arise from a pathogen that is restricted to the stratum corneum, with little or no tissue reaction • Important superficial mycoses are Tinea versicolor, Piedra and Tinea nigra • Tinea versicolor (Pityriasis versicolor) o It is a superficial chronic infection of stratum corneum o It is common worldwide and is caused by Malassezia spp, which are human saprophytes that sometimes switch from yeast to pathogenic mold forms o Three species of Malassezia are linked to tinea versicolor; ▪ Malassezia furfur ▪ Malassezia globose ▪ Malassezia sympodialis o Signs and symptoms are; ▪ Hyperpigmented or depigmented maculae on chest, back, arms and abdomen ▪ Does not illicit immune response, no discomfort ▪ Limited to the stratum corneum o Treatment ▪ Topical antifungal e.g. whitfield’s ointment, miconazole, itraconazole ▪ Oral azole • Piedra o (White and black piedra) is common in tropical regions of the world o White piedra is also endemic in temperate climates o Black piedra is caused by Piedraia hortae o White piedra is a superficial fungal infection of the hair shaft is caused by Trichosporon species e.g. Trichosporon beigelii o Signs and symptoms ▪ White piedra shows irregular, white, cream-colored, or brown soft nodules or gelatinous sheaths along the hair shaft ▪ They can be easily detached from

NTA Level 5 • Semester 1 • PST05103 Opportunistic Mycoses Pharmaceutical Microbiology • Source Session/Topic 35 Full source-text version: all educational wording from the extracted learning source is retained; only presenter/tutor metadata and web-layout noise are removed, while formatting is improved for readability. Session 35: Opportunistic Mycoses Total Session Time: 120 minutes Pre-requisites • Human anatomy and physiology Students Learning Tasks By the end of this session students are expected to be able to: • Classify and describe Oppotunistic mycoses (causative agents, transmission, signs and symptoms) • Describe treatment, prevention and control of oppotunistic mycoses Resources Needed: • Flip charts, marker pens, and masking tape • Black/white board and chalk/whiteboard markers SESSION OVERVIEW |Step |Time |Activity/ |Content | | | |Method | | |1 |5 minutes |Presentation |Introduction, Learning Tasks | |2 |20 minutes |Presentation |Introduction to Opportunistic | | | | |Mycoses | |3 |30 minutes |Presentation |Candidiasis | |4 |20 minutes |Presentation |Cryptococcosis | |5 |30 minutes |Presentation |Pneumocystis Pneumonia | |6 |5 minutes |Presentation |Key Points | | 7|5 minutes |Presentation |Evaluation | SESSION CONTENTS STEP 1: Presentation of Session Title and Learning Tasks (5 minutes) READ or ASK students to read the learning tasks and clarify ASK students if they have any questions before continuing STEP 2: Introduction to Opportunistic Mycoses (20 minutes) • Opportunistic mycoses are fungal infections that occur immunocompromised patients • The common causes of immunocompromised immunity include AIDS, azotemia, diabetes mellitus, lymphoma, leukemia, other hematologic cancers, burns, and therapy with corticosteroids, immunosuppressants, or antimetabolites • Patients who spend more than several days in an ICU can become compromised because of medical procedures, underlying disorders, and/or undernutrition • Fungi which cause opportunistic mycoses include Candida albicans, Cryptococcus neoformans, Coccidioides immitis, Histoplasma capsulatum, Pneumocystis jiroveci • Systemic mycoses affecting severely immunocompromised patients often manifest acutely with rapidly progressive pneumonia, fungemia, or manifestations of extrapulmonary dissemination. STEP 3: Candidiasis (30 minutes) • Cause and Transmission o Candidiasis is an opportunistic mycosis and the most the most prevalent systemic mycosis caused mainly by Candida albicans o Other Candida species causing candidiasis include Candida parapsilosis, Candida glabrata, Candida tropicalis, Candida guilliermondii, and Candida dubliniensis o Candida species are members of the normal flora of the skin, mucous membranes, and gastrointestinal tract o Candida species colonize the mucosal surfaces of all humans soon after birth, and the risk of endogenous infection is ever present. o Candidiasis is usually precipitated by prolonged use of contraceptive pills, AIDS, pregnancy, diabetes, prolonged use of antibiotics, corticosteroid use, and immunosuppressive treatment o Candida species cause both cutaneous or mucocutaneous and systemic opportunistic infections • The signs and symptoms o Cutaneous and mucosal candidiasis ▪ Oral thrush • Oral lesions characterized by white, adherent mucosal plaques (a patchy to confluent, whitish pseudomembrane) on the lips, gums, tongue or the palate ▪ Vaginal candidiasis (vulvovaginitis) • Itchy, curd-like whitish vaginal discharge, dysuria and dyspareunia ▪ Cutaneous candidiasis • Erythematous, moist exudate in the skin folds and accompanying satellite pustules ▪ Onychomycosis • Painful swelling of the nail bed and folds, with pus discharge and is made worse by contact with water ▪ Gastrointestinal candidiasis • Painful swallowing (odynophagia) • Characteristic lesions are seen on endoscopy ▪ Systemic candidiasis • Occult lesions develop anywhere, especially the kidney, skin (maculonodular lesions), eye, heart, and meninges • Treatment and Prevention o Cutaneous candidiasis ▪ Topical clotrimazole ▪ Topical miconazole o Oral candidiasis ▪ Nystatin oral suspension o Vaginal candidiasis ▪ Nystatin (vagina) pessaries ▪ Miconazole (vaginal) pessaries ▪ Systemic fluconazole o Gastrointestinal candidiasis ▪ Systemic fluconazole o Prevention ▪ Avoid disturbing microbial normal flora STEP 4: Cryptococcosis (20 minutes) • Cause and Transmission o Cryptococcus neoformans causes cryptococcosis which is a fungal infection of the brain resulting in Cryptococcal meningoencephalitis. o C neoformans occurs in immunocompetent persons but more often in patients with HIV/AIDS, haematogenous malignancies, and other immunosuppressive conditions o C. neoformans commonly found in avian faeces, is transmitted through inhalation of desiccated yeasts (or basidiospores) to pulmonary alveoli o Infection is initiated by inhalation of the yeast cells, which in nature are dry, minimally encapsulated, and easily aerosolized o The primary pulmonary infection may be asymptomatic or may mimic an influenza-like respiratory infection, often resolving spontaneously o In immunocompromised patients the yeasts may multiply and disseminate to other parts of the body but preferentially to the central nervous system, causing cryptococcal meningoencephalitis • Signs and Symptoms o Headache o neck stiffness o Disorientation o There may be lesions in skin, lungs, or other organs o Chronic meningitis, (which can resemble a brain tumour, brain abscess, degenerative central nervous system disease, or any mycobacterial or fungal meningitis) • Treatment and Prevention o Combination therapy ▪ Amphotericin B and Flucytosine o Prevention ▪ Care in handling avian faeces STEP 5: Pneumocystis Pneumonia (20 minutes) • This is fungal pneumonia caused by Pneumocystis jiroveci in immunocompromised patients • P. jiroveci was thought to be a protozoan for many years, but now proven to be a fungus with a close relationship to ascomycetes • Pneumocystis species are present in the lungs of many animals (rats, mice, dogs, cats, ferrets, rabbits) but rarely cause disease unless the host is immunosuppressed • Pneumocystis carinii is found only in rats • Before the introduction of effective chemoprophylactic regimens, this disease was a major cause of death among AIDS patients • The disease is acquired through inhalation • Acute cases of Pneumocystis pneumonia are treated with trimethoprim- sulfamethoxazole or pentamidine isethionate • Prophylaxis can be achieved with daily Trimethoprime/Sulfamethoxazole (Co-trimoxazole) or aerosolized pentamidine STEP 6: Key Points (5 minutes) • Opportunistic mycoses are caused by globally distributed fungi that are either members of the human microbiota, such as Candida species, or environmental yeasts and moulds • Among the categories of fungal infections, the incidence, severity, and mortality of systemic opportunistic mycoses are the highest • Most patients with HIV/AIDS develop mucosal candidiasis (e.g. thrush, esophagitis) • HIV/AIDS patients with CD4 counts less than 100 cells/μL are at risk for cryptococcosis, pneumocystis pneumonia,

NTA Level 5 • Semester 1 • PST05103 Introductory Parasitology Pharmaceutical Microbiology • Source Session/Topic 36 Full source-text version: all educational wording from the extracted learning source is retained; only presenter/tutor metadata and web-layout noise are removed, while formatting is improved for readability. Session 36: Introductory Parasitology Total Session Time: 60 minutes Pre-requisites • Human anatomy and physiology Students Learning Tasks By the end of this session students are expected to be able to: • Define common terms used in parasitology • Classify and list general characteristics of parasites Resources Needed: • Flip charts, marker pens, and masking tape • Black/white board and chalk/whiteboard markers SESSION OVERVIEW |Step |Time |Activity/ |Content | | | |Method | | |1 |5 minutes |Presentation |Introduction, Learning Tasks | |2 | 15 minutes|Presentation |Common Terms used in Parasitology | |3 |30 minutes |Presentation |Classification of and General | | | | |Characteristics of Medical | | | | |Parasites | |4 |5 minutes |Presentation |Key Points | | 5|5 minutes |Presentation |Evaluation | SESSION CONTENTS STEP 1: Presentation of Session Title and Learning Tasks (5 minutes) READ or ASK students to read the learning tasks and clarify ASK students if they have any questions before continuing STEP 2: Common Terms used in Parasitology (15 minutes) • Parasitology o Parasitology is the study of parasites that infect humans. Parasitology deals with characteristics, transmission, clinical features and diagnosis, treatment and prevention of diseases caused by the parasites. • Parasite o A parasite is an organism that depends on another organism (a host) for food, shelter or other benefits and which receives these benefits is such a way that the host experience detrimental effects as a consequence. It is simply an organism that depends on other organisms and at the same time causing harm to that organism. o Examples of parasites included in parasitology are protozoa, helminthes, and some arthopods. • Host o A host is an organism that harbours the parasite • Intermediate host o Is a host that harbours the larval or asexual stages of the parasite. Sometimes larval development is completed in two different intermediate hosts, referred to as first and second intermediate hosts • Definitive host o Is a host that either harbors the adult stage of the parasite or where the parasite utilizes the sexual method of reproduction. In the majority of human parasitic infections, man is the definitive host except for example in malaria however, man acts as the intermediate host. • Ectoparasite o A parasite that lives on the outer surface of its host e.g. lice, ticks. • Endoparasite o A parasite that lives inside the body of its host e.g. Entamoeba histolytica • Obligate parasite o Is a parasite that completely depends on the host during a segment or all of its life cycle e.g. Plasmodium species. • Facultative parasite o Is an organism that exhibits both parasitic and non-parasitic modes of living and therefore does not absolutely depend on the parasitic way of life but is capable of adopting it if placed in a host • Erratic parasite o Is a parasite that wonders in to an organism in which it is not usually found e.g. Entamoeba histolytica in the liver or lungs of humans • Symbiosis o Is an association in which both the parasite and the host are so dependent upon each other that one cannot live without the other and none suffers any harm from the association • Commensalisms o This is an association in which only the parasite derives benefit from the association but without causing injury to its host. • Parasitism o This is an association in which the parasite derives benefit and the host gets nothing in return but always suffers some injury • Encystation o This is the transformation of a parasite from an active (trophozoite) to an inactive stage through losing its power of motility and enclosing itself within a tough wall (cyst). o The cyst is the resistant stage of the parasite and is also infective to its human host. • Extrinsic incubation period o This is the interval between the acquision of an infectious agent by a vector and the vector’s ability to transmit the agent to other susceptible vertebrate host • Carrier state o A perfect host-parasite relationship where tissue destruction by a parasite is balanced with host’s tissue repair STEP 3: Classification and General Characteristics of Medical Parasites (30 minutes) General Characteristics • Parasites have multiple life stages o Because of this they exhibit different immune response, makes it difficult to formulate vaccines and are difficult to control • Parasites spend part of their life cycle within or on a host body; • Parasites require sustenance from the host in order to survive in the period it is within or on the host • Parasites can be ectoparasites or endoparasites • Some parasites are unicellular parasites (protozoa) while others are multicellular (helminths and arthropods) Classification of Medical Parasites • Medical parasites can be grouped into protozoa, helminths, and ectoparasites. • Protozoa o Protozoa are microscopic, unicellular organisms that can be free- living or parasitic in nature o Protozoans are eukaryotic o They are made up of cytoplasm and nucleus ▪ Cytoplasm is differentiated into endoplasm and ectoplasm ▪ Nucleus contains karyosome and peripheral chromatin o They are able to multiply in humans, which contributes to their survival and also permits serious infections to develop from just a single organism o Transmission of protozoa that live in a human’s intestine to another human typically occurs through a fecal-oral route (for example, contaminated food or water or person-to-person contact). o Protozoa that live in the blood or tissue of humans are transmitted to other humans by an arthropod vector (for example, through the bite of a mosquito or sand fly) o The protozoa that are infectious to humans can be classified into four groups based on their mode of movement; ▪ Sarcodina (pseudopods) • Belong to phylum Sarcomastigophora • Move by pseudopodia, e.g. Amoeba such as Entamoeba

NTA Level 5 • Semester 1 • PST05103 Blood and Tissue Protozoal Infections Pharmaceutical Microbiology • Source Session/Topic 37 Full source-text version: all educational wording from the extracted learning source is retained; only presenter/tutor metadata and web-layout noise are removed, while formatting is improved for readability. Session 37: Blood and Tissue Protozoal Infections Total Session Time: 120 minutes Pre-requisites • Human anatomy and physiology Students Learning Tasks By the end of this session students are expected to be able to: • Describe causative agents, transmission, life cycle, signs/symptoms of Malaria, Toxoplamosis andTrypanosomiasis Resources Needed: • Flip charts, marker pens, and masking tape • Black/white board and chalk/whiteboard markers SESSION OVERVIEW |Step |Time |Activity/ |Content | | | |Method | | |1 |5 minutes |Presentation |Introduction, Learning Tasks | |2 | |Small group |Malaria | | |40 minutes |discussion/ | | | | |Presentation | | |3 | 35 |Presentation |Toxoplasmosis | | |minutes | | | |4 |30 minutes |Presentation |African Trypanosomiasis | |5 |5 minutes |Presentation |Key Points | | 6|5 minutes |Presentation |Evaluation | SESSION CONTENTS STEP 1: Presentation of Session Title and Learning Tasks (5 minutes) READ or ASK students to read the learning tasks and clarify ASK students if they have any questions before continuing STEP 2: Malaria (40 minutes) Cause and Transmission • Malaria is a life-threatening mosquito-borne blood disease caused by various species of Plasmodium • Species of Plasmodium causing malaria include: o Plasmodium falciparum o Plasmodium vivax o Plasmodium ovale o Plasmodium malariae o Plasmodium knowlesi • Severity of malaria depends on the species involved • Malaria is transmitted by the bite of an infected female Anopheles mosquito. • Life cycle of Plasmodium o The malaria parasite life cycle involves two hosts. o During a blood meal, a malaria-infected female Anopheles mosquito inoculates sporozoites into the human host o Sporozoites infect liver cells and mature into schizonts, which rupture and release (merozoites (In P. vivax and P. ovale a dormant stage (hypnozoites) can persist in the liver and cause relapses by invading the bloodstream weeks, or even years later.) o After this initial replication in the liver (exo-erythrocytic schizogony), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony). o Merozoites infect red blood cells. o The ring stage trophozoites mature into schizonts, which rupture releasing merozoites o Some parasites differentiate into sexual erythrocytic stages (gametocytes) o Blood stage parasites are responsible for the clinical manifestations of the disease. The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by an Anopheles mosquito during a blood meal o The parasites’ multiplication in the mosquito is known as the sporogonic cycle o While in the mosquito’s stomach, the microgametes penetrate the macrogametes generating zygotes o The zygotes in turn become motile and elongated (ookinetes) which invade the midgut wall of the mosquito where they develop into oocysts o The oocysts grow, rupture, and release sporozoites, which make their way to the mosquito’s salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle. [pic] • Types of malaria o The disease presentation will vary according to patient’s state of immunity, the intensity of the infection and the presence of accompany conditions such as malnutrition, anaemia and other diseases. ▪ Uncomplicated Malaria • Uncomplicated malaria is defined as symptomatic malaria without signs of severity or evidence (clinical or laboratory) of vital organ dysfunction. • In this type of malaria, symptoms are present, but there are no signs to indicate severe infection or dysfunction of the vital organs. • This form can become severe malaria if left untreated, or if the host has poor or no immunity. ▪ Severe Malaria • Severe malaria is symptomatic malaria with signs of severity of vial organ dysfunction. Severe Plasmodium falciparum malaria is a medical emergency. • In severe malaria, clinical or laboratory evidence shows signs of vital organ dysfunction • Delay in diagnosis and provision of appropriate treatment may lead to serious complications and even death Signs and Symptoms • Signs and symptoms of uncomplicated malaria o Fever, headache, nausea, vomiting, o Malaise, fatigue, muscle pain, o Anorexia, chill, rigors, sweats, cough and diarrhea • Signs and symptoms of severe malaria o Fever and chills o Impaired consciousness o Change in behavior o Prostration/extreme weakness o Respiratory distress o Circulatory collapse/shock o Vomiting everything o Multiple convulsions o Deep breathing and respiratory distress o Abnormal bleeding and signs of anemia o Clinical jaundice and evidence of vital organ dysfunction o Severe malaria can be fatal without treatment o Inability to drink or breastfeed o Complications of severe malaria include; ▪ Hyperpyrexia, convulsions, shock, hypoglycaemia, metabolic acidosis, acute renal failure or pulmonary oedema o In Tanzania the commonest presentations of severe malaria are; ▪ Severe anaemia ▪ Coma (cerebral Malaria) Treatment and Prevention • Treatment of Uncomplicated Malaria o Artemisinin-based combination therapy (ACT) is recommended by the WHO to treat uncomplicated malaria. o ACT is artemisinin combined with a partner drug. The role of artemisinin is to reduce the number of parasites within the first 3 days of infection, while the partner drugs eliminate the rest. o These drugs include; ▪ Artemether-Lumefanthrine ▪ Dihydroartemisinin with Piperaquine ▪ Uncomplicated malaria in first trimester of pregnancy is managed by quinine tablet • Treatment of Severe Malaria o Hypoglycaemia is the major problem in the management of severe malaria especially in young children and pregnant women. Hypoglycaemia should be looked and treated accordingly. Other features like anaemia should also be addressed ▪ Medications include: • Quinine injection • Artesunate injection |Activity: Take home Assignment (10 minutes) | | | |DIVIDE students in groups or individual. | | | |ASK the students to work on the following assignment | | | |Explain the dose and dosing schedule for antimalarial drugs used in | |the treatment of uncomplicated and severe malaria in Tanzania | | | |ALLOCATE time for students to do the assignment and submit | | | |REFER students to recommended references | • Prevention of Malaria |Activity:

NTA Level 5 • Semester 1 • PST05103 Intestinal and Urinogenital Protozoal Infections Pharmaceutical Microbiology • Source Session/Topic 38 Full source-text version: all educational wording from the extracted learning source is retained; only presenter/tutor metadata and web-layout noise are removed, while formatting is improved for readability. Session 38: Intestinal and Urinogenital Protozoal Infections Total Session Time: 120 minutes Pre-requisites • Human anatomy and physiology Students Learning Tasks By the end of this session students are expected to be able to: • Describe causative agents, transmission, life cycle, signs/symptoms of common diseases caused by intestinal and urinogenital protozoa (Giardiasis, Amoebiasis, Cryptosporidiosis, Trichomoniasis) • Describe treatment, prevention and control of common intestinal and urinogenital protozoa diseases Resources Needed: • Flip charts, marker pens, and masking tape • Black/white board and chalk/whiteboard markers SESSION OVERVIEW |Step |Time |Activity/ |Content | | | |Method | | |1 |5 minutes |Presentatio|Introduction, Learning Tasks | | | |n | | |2 |30 minutes |Presentatio|Giardiasis | | | |n | | |3 |35 minutes |Buzzing/ |Amoebiasis | | | |Presentatio| | | | |n | | |4 |20 minutes |Presentatio|Cryptosporidiosis | | | |n | | |5 |20 minutes |Presentatio|Trichomoniasis | | | |n | | |6 |5 minutes |Presentatio|Key Points | | | |n | | |7 |5 minutes |Presentatio|Evaluation | | | |n | | SESSION CONTENTS STEP 1: Presentation of Session Title and Learning Tasks (5 minutes) READ or ASK students to read the learning tasks and clarify ASK students if they have any questions before continuing STEP 2: Giardiasis (30 minutes) • Cause and Transmission o It is the infestation of the upper small intestine caused by the flagellate protozoan Giardia Lamblia (or G. intestinalis), cytopathic effects of which leads to malabsorption and diarrhea o Giardiasis can be asymptomatic or cause symptoms ranging from intermittent flatulence to chronic malabsorption o Giardiasis is transmitted through faecal-oral route by ingestion of faecal contaminated food or water. o Life cycle ▪ Giardia cysts are the infective stage of G. intestinalis ▪ These cysts are ingested by consuming contaminated food or water, or fecal-orally ▪ Cysts excyt in in the low pH of the stomach acid releases trophozoites, with each cyst producing two trophozoites ▪ Within the small intestine, the trophozoites reproduce asexually and either float free or are attached to the mucosa of the lumen ▪ Some trophozoites then encyst in the small intestine ▪ Both cysts and trophozoites are then passed in the faeces, and are infectious immediately or shortly afterward ▪ Person-to-person transmission is possible [pic] • Signs and Symptoms o Abdominal cramps o Abdominal distension o Flatulence o Intermittent nausea o Epigastric discomfort o Chronic Diarrhoea o Steatorrhea due to malabsorption o Anorexia o weight loss • Treatment and Prevention o Treatment ▪ Metronidazole ▪ Tinidazole ▪ Secnidazole o Prevention ▪ Personal hygiene ▪ Hygienic food handling STEP 3: Amoebiasis (35 minutes) • Cause and Transmission o Amoebiasis is an infection caused by the protozoa organism Entamoeba histolytica, which can cause colitis and other extra-intestinal manifestations o It is commonly asymptomatic, but symptoms ranging from mild diarrhoea to severe dysentery may occur o The infection is primarily acquired through ingestion of contaminated food and water and occasionally can be acquired through oral-anal sexual practices o Life cycle ▪ Cysts and trophozoites are passed in faeces ▪ Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool ▪ Infection by Entamoeba histolytica occurs by ingestion of mature cysts in faecally contaminated food, water, or hands ▪ Excystation occurs in the small intestine and trophozoites are released, which migrate to the large intestine ▪ The trophozoites multiply by binary fission and produce cysts The Number 5, and both stages are passed in the faeces ▪ Because of the protection conferred by their walls, the cysts can survive days to weeks in the external environment and are responsible for transmission ▪ Trophozoites passed in the stool are rapidly destroyed once outside the body, and if ingested would not survive exposure to the gastric environment ▪ In many cases, the trophozoites remain confined to the intestinal lumen (non-invasive infection) of individuals who are asymptomatic carriers, passing cysts in their stool ▪ In some patients the trophozoites invade the intestinal mucosa (Intestinal disease), or through the bloodstream, extraintestinal sites such as the liver, brain, and lungs (extraintestinal amoebiasis), with resultant pathologic manifestations • Extraintestinal amoebiasis o Liver abscess o Cutaneous amoebiasis [pic] • Signs and Symptoms • |Activity: Buzzing (5 minutes) | | | |ASK students to pair up and buzz on the following question for 2 | |minutes | | | |What are the signs and symptoms of amoebiasis? | | | |ALLOW few pairs to respond and let other pairs to add on points | |not mentioned | | | |WRITE their response on the flip chart/board | | | |CLARIFY and SUMMARIZE by using the content below | o Bloody diarrhoea o Crampy abdominal pain o Tenesmus (Irresistible urge to go to the toilet) o Fever o Weight loss o Peritonitis in severe forms o Evidence of motile trophozoites or cysts on saline wet mount from a stool specimen • Extraintestinal Amoebiasis o Extraintestinal amoebic disease originates from infection in the colon and can involve any organ, but a liver abscess is the most common o Liver Abscess • High grade fever, sweats and chills • Nausea, vomiting • Weakness and weight loss • Right upper quadrant pain • Tender and enlarged liver • The abscess may perforate into the subphrenic space, right pleural cavity, right lung, or other adjacent organs (e.g. pericardium) o Cutaneous Amoebiasis (Skin lesions) • Occasionally observed, especially around the perineum and buttocks in chronic infection, and may also occur in traumatic or operative wounds • Treatment and Prevention o Treatment ▪ Use of nitroimidazoles o Metronidazole o Tinidazole o Secnidazole o Prevention ▪ Personal hygiene e.g. washing hands after using toilet and before eating ▪ Food hygiene ▪ Hygienic food preparation and handling ▪

NTA Level 5 • Semester 1 • PST05103 Taeniasis and Schistosomiasis Pharmaceutical Microbiology • Source Session/Topic 39 Full source-text version: all educational wording from the extracted learning source is retained; only presenter/tutor metadata and web-layout noise are removed, while formatting is improved for readability. Session 39: Taeniasis and Schistosomiasis Total Session Time: 120 minutes Pre-requisites • Human anatomy and physiology Students Learning Tasks By the end of this session students are expected to be able to: • Describe taeniasis and schistosoniasis basing oncausative agents, transmission, life cycle, signs/symptoms of common diseases caused by helminths (Taenia, Schistosoma, pinworm, whipworm, hookworm, intestinal roundworm, filarial worm) • Describe treatment,prevention and control of taeniasis and schistosomiasis Resources Needed: • Flip charts, marker pens, and masking tape • Black/white board and chalk/whiteboard markers SESSION OVERVIEW |Step |Time |Activity/ |Content | | | |Method | | |1 |5 minutes |Presentation |Introduction, Learning Tasks | |2 | 15 minutes|Presentation |Taeniasis and Cysticercosis | |3 |30 minutes |Buzzing/ |Schistosomiasis | | | |Presentation | | |4 |5 minutes |Presentation |Key Points | | 5|5 minutes |Presentation |Evaluation | SESSION CONTENTS STEP 1: Presentation of Session Title and Learning Tasks (5 minutes) READ or ASK students to read the learning tasks and clarify ASK students if they have any questions before continuing STEP 2: Taeniasis and Cysticercosis (15 minutes) Cause and Transmission • Taeniasis is a tapeworm disease caused by Taenia saginata (beef tapeworm), Taenia solium (pork tapeworm), Diphyllobothrium latum (fish tapeworm) and Hymenolepsis nana. Teaniasis leads to chronic malnutrition or multi-organ dissemination and dysfunction (Cysticercosis) • Humans are the only hosts for these Taenia tapeworms. • Taeniasis is transmitted through consumption of raw or undercooked beef or pork containing infective cysticerci of the worms. • T. solium also causes cysticercosis which is a parasitic tissue infection caused by larval cysts of the tapeworm and is transmitted by consumption of eggs of the worms. Life cycle • Taeniasis is the infection of humans with the adult tapeworm of Taenia saginata or Taenia solium • Humans are the only definitive hosts for T. saginata and T. solium. Eggs or gravid proglottids are passed with feces; the eggs can survive for days to months in the environment. • Cattle (T. saginata) and pigs (T. solium) become infected by ingesting vegetation contaminated with eggs or gravid proglottids • In the animal’s intestine, the oncospheres hatch, invade the intestinal wall, and migrate to the striated muscles, where they develop into cysticerci. • A cysticercus can survive for several years in the animal. Humans become infected by ingesting raw or undercooked infected meat. • In the human intestine, the cysticercus develops over 2 months into an adult tapeworm, which can survive for years. • The adult tapeworms attach to the small intestine by their scolex and reside in the small intestine • Length of adult worms is usually 5 m or less for T. saginata (however it may reach up to 25 m) and 2 to 7 m for T. solium. • The adults produce proglottids which mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool (approximately 6 per day). T. saginata adults usually have 1,000 to 2,000 proglottids, while T. solium adults have an average of 1,000 proglottids. • The eggs contained in the gravid proglottids are released after the proglottids are passed with the feces. T. saginata may produce up to 100,000 and T. solium may produce 50,000 eggs per proglottid respectively. Taeniasis (T. saginata and T. solium) [pic] Cysticercosis (T. solium) [pic] • Signs and Symptoms of Taeniasis o Most people have no symptoms or have mild symptoms o Colicky abdominal pain o Body Weakness o Loss of or increased appetite o Constipation or diarrhea o Mild epigastric discomfort o Nausea o Weight loss o Abdominal pain o Pruritus ani o Hyperexcitability • Infection with T. solium tapeworms can result in human cysticercosis • Cysticercosis is a parasitic tissue infection caused by larval cysts of the tapeworm Taenia solium. The larval cysts infect brain, muscle, or other tissue (see life cycle). Cysticercosis is transmitted by swallowing eggs found in the feces of a person infested with T.solium, e.g. autoinfection with own fingers o The cysticerci are most often located in subcutaneous and intermuscular tissues, followed by the eye and then the brain. o The CNS is involved in 60-90% of patients i.e. Neurocystercosis (cysticercosis of the brain) which may manifest as; ▪ Convulsions and/or seizures ▪ Intracranial hypertension • Headache, nausea, vomiting, vertigo, and papilledema • Personality and mental status changes (Neuropsychiatric changes) • Behavioral changes and learning disabilities more marked in children and immunocompromised adults • Treatment and Prevention o Taeniasis ▪ Praziquantel or Niclosamide with Magnesium sulphate (oral) o Cysticercosis ▪ Praziquantel or Albendazole with Dexamethasone and Carbamazepine (oral) • Taeniasis and cysticercosis are prevented by; o Health education o Avoid eating raw pork o Sanitary inspection of slaughter houses STEP 3: Schistosomiasis (30 minutes) • Cause and Transmission o Schistosomiasis (also known as bilharzia) is a parasitic disease caused by blood flukes (trematodes) of the genus Schistosoma ▪ Three species of Schistosoma are commonly found in Tanzania; • Schistosoma haematobium –responsible mainly for urogenital Schistosomiasis • Schistosoma mansoni –responsible mainly for intestinal Schistosomiasis. • Scistosoma japonicum responsible for both of intestinal and urinogenital schistosomiasis o Schistosoma parasites are transmitted to humans through skin penetration of the cercariae (infective forms of Schistosoma) when humans are in contact with contaminated freshwater. o Life cycle; ▪ Eggs are eliminated with feces or urine and hatch to release miracidia, which swim and penetrate specific snail (Bullinus) intermediate hosts ▪ The stages in the snail include 2 generations of sporocysts and the production of cercariae, which are the infective forms. Upon release from the snail, the cercariae swim, penetrate the skin of the human host and shed their forked tail, becoming schistosomulae. ▪ The schistosomulae migrate through several tissues and stages to their residence in the veins ▪ Adult worms in humans reside

NTA Level 5 • Semester 1 • PST05103 Pinworm, Whipworm, Hookworm and Roundworm Infestations Pharmaceutical Microbiology • Source Session/Topic 40 Full source-text version: all educational wording from the extracted learning source is retained; only presenter/tutor metadata and web-layout noise are removed, while formatting is improved for readability. Session 40: Pinworm, Whipworm, Hookworm and Roundworm Infestations Total Session Time: 120 minutes Pre-requisites • Human anatomy and physiology Students Learning Tasks By the end of this session students are expected to be able to: • Describe causative agents, transmission, life cycle, signs/symptoms of common diseases caused by helminths (, pinworm, whipworm, hookworm, intestinal roundworm, filarial worm) • Describe treatment, prevention and control of pinworm, whipworm, hookworm, intestinal roundworm, filarial worm) • Resources Needed: • Flip charts, marker pens, and masking tape • Black/white board and chalk/whiteboard markers SESSION OVERVIEW |Step |Time |Activity/ |Content | | | |Method | | |1 |5 minutes |Presentation |Introduction, Learning Tasks | |2 |25 minutes |Presentation |Pinworm infestation (Enterobiasis)| |3 |25 minutes |Presentation |Whipworm infestation | | | | |(Trichuriasis) | |4 |25 minutes |Presentation |Hookworm infestation | | | | |(Ancylostomiasis) | |5 |30 minutes |Presentation |Roundworm infestation (Ascariasis)| |6 |5 minutes |Presentation |Key Points | | 7|5 minutes |Presentation |Evaluation | SESSION CONTENTS STEP 1: Presentation of Session Title and Learning Tasks (5 minutes) READ or ASK students to read the learning tasks and clarify ASK students if they have any questions before continuing STEP 2: Pinworm Infestation –Enterobiasis (15 minutes) Cause and Transmission • Pinworm infection (also known as enterobiasis), is a human parasitic disease caused by the pinworm Enterobius vermicularis. • E. vermicularis is an intestinal nematode that is tiny, white and spindle-shaped with a large, bulbar esophagus • Enterobiasis is transmitted by the faecal-oral route, either directly or indirectly via contaminated hands or objects such as clothes, toys, and bedding. • The disease is more common in children • Females usually migrate out the anus at night and depositeggs on the perianal skin. • The eggs embryonate quickly and, if ingested, hatch and mature in the intestines. • Life cycle o Eggs are deposited on perianal folds. Self-infection occurs by transferring infective eggs to the mouth with hands that have scratched the perianal area. o Person-to-person transmission can also occur through handling of contaminated clothes or bed linens. o Enterobiasis may also be acquired through surfaces in the environment that are contaminated with pinworm eggs (e.g. curtains, carpeting). o Some small number of eggs may become airborne and inhaled. These would be swallowed and follow the same development as ingested eggs. o Following ingestion of infective eggs, the larvae hatch in the small intestine and the adults establish themselves in the colon o The time interval from ingestion of infective eggs to oviposition by the adult females is about one month. o The life span of the adults is about two months. Gravid females migrate nocturnally outside the anus and oviposit while crawling on the skin of the perianal area. o The larvae contained inside the eggs develop (the eggs become infective) in 4 to 6 hours under optimal conditions. o Retroinfection, or the migration of newly hatched larvae from the anal skin back into the rectum, may occur [pic] • Signs and Symptoms o Enterobiasis is most common in children, who usually present with ▪ Pruritus ani ▪ Insomnia (sometimes) ▪ Abdominal pain ▪ Anorexia, and pallor ▪ Genitourinary infection may occur in females. • Treatment and Prevention o Antihelminthic drugs ▪ Mebendazole ▪ Pyrantel pamoate ▪ Albendazole o Preventive measures include; ▪ Treatment of the sick and carriers ▪ Improved personal hygiene, including washing the perianal region and changing nightclothes STEP 3: Whipworm Infestation –Trichuriasis (30 minutes) Cause and Transmission • Trichuriasis is a parasitic disease caused by infection of the large intestine by Trichuris trichiura (also known as the human whipworm), which is an intestinal parasitic nematode. • Adult whipworms mainly live in the caecum, but can be seen throughout the colon and rectum. People infected with whipworm can suffer light or heavy infections. • T. trichjura belongs to the family Trichuridae. The worms are known as "whip-worms" because they have a broad short posterior end and a very long narrow whip-like anterior end • Trichuriasis is transmitted by the faecal-oral route, involving the ingestion of eggs with contaminated food, water or soil. • Life cycle o The unembryonated eggs are passed with the stool. In the soil, the eggs develop into a 2-cell stage, an advanced cleavage stage, and then they embryonate; eggs become infective in 15 to 30 days. o After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine, and release larvae that mature and establish themselves as adults in the colon. o The adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The adult worms are fixed in that location, with the anterior portions threaded into the mucosa. o The females begin to oviposit 60 to 70 days after infection. Female worms in the cecum shed between 3,000 and 20,000 eggs per day. The life span of the adults is about 1 year. [pic] Signs and Symptoms • Heavy infections may cause dysentery, anaemia, malnutrition, and occasionally rectal prolapse Treatment and Prevention • Anthelminthic medications o Albendazole o Mebendazole • Infections are generally treated for 3 days. • Trichuriasis is prevented b; o Sanitary disposal of faeces o Effective sewage disposal systems o Personal hygiene e.g. washing hands o Thorough washing of vegetables, salads and fruits with clean water prior to consumption STEP 4: Hookworm Infestation –Ancylostomiasis (30 minutes) Ancylostomiasis • Human hookworm or ancylostomiasis is a hookworm disease caused by infestation of the small intestine with Ancylostoma duodenale or Necator americanus. It is one of the main causes of anaemia in the tropics which is also the major clinical feature. • Life cycle o Eggs are passed in the stool and under favorable conditions (moisture, warmth, shade), larvae hatch in 1 to 2 days to