PST05103 Pharmaceutical Microbiology

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 Measles and Poliomyelitis Pharmaceutical Microbiology • Source Session/Topic 26 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 26: Measles and Poliomyelitis 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 Measle and poliomyelitis (causative agents, transmission, signs and symptoms) • Describe treatment, prevention and control of Measle and poliomyelitis 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 |Measles | |3 |20 minutes |Presentation |Poliomyelitis | |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: Measles (25 minutes) • Measles is an acute, highly communicable infectious disease caused by Measles virus. • The mode of transmission is airborne, by droplet spread through coughing or sneezing or by direct contact with nasal or throat secretions of infected persons • Signs and Symptoms o Generalized, reddish (erythematous), blotchy (maculopapular) rash; o History of fever usually above 38˚C (if not measured, then "hot" to touch) o Dry cough, sore throat, runny nose (coryza) o Inflamed eyes (conjunctivitis), tiny white spots with bluish-white centers on a red background found inside the mouth on the inner lining of the cheek- also called Koplik's spots o In addition, children with measles frequently exhibit a dislike of bright light (photophobia), and often have a sore red mouth (stomatitis) • Treatment o No specific antiviral treatment exists for measles virus o Paracetamol o Vitamin A o Oxyetracycline ointment (for ocular involvement) • Prevention o Immunization with measles vaccine STEP 3: Poliomyelitis (20 minutes) • Poliomyelitis is an acute infection caused by a poliovirus (an enterovirus) • Humans are the only natural host • Asymptomatic and minor infections (abortive poliomyelitis) are more common than non-paralytic or paralytic infections by ≥ 60:1 and are the main source of spread • The virus enters via the faecal-oral or respiratory route, then enters the lymphoid tissues of the GI tract • A primary (minor) viremia follows with spread of virus to the reticuloendothelial system • Signs and symptoms include; o A nonspecific minor illness (abortive poliomyelitis), sometimes aseptic meningitis without paralysis (non-paralytic poliomyelitis), and, less often, flaccid weakness of various muscle groups (paralytic poliomyelitis) • Treatment o Supportive • Prevention o Immunization STEP 4: Key Points (5 minutes) • Measles is an acute, highly communicable infectious disease caused by Measles virus. And transmitted via respiratory droplets • Important signs and symptoms of measles are cough, runny nose, conjunctivitis and photophobia • Poliomyelitis is a debilitating disease caused by poliovirus and transmitted via faecal-oral route or respiratory route • Both measles and poliomyelitis do have specific treatment and prevented by immunization STEP 5: Evaluation (5 minutes) • What are the effects of poliomyelitis? • How is measles prevented? 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 ← Previous TopicNext Topic →View all Pharmaceutical Microbiology topicsOpen Complete Full Notes PDF / OFFLINE NOTES Unataka kutumiwa notes hizi kupitia WhatsApp?Kwa notes zilizopangiliwa vizuri kwa kusoma offline au PDF, bonyeza kitufe hapa chini. Ujumbe wenye Level, Semester, Module na Topic utaandaliwa moja kwa moja.TUMIWA NOTES WHATSAPP WhatsApp: 255620339260

NTA Level 5 • Semester 1 • PST05103 Viral Hepatitis Pharmaceutical Microbiology • Source Session/Topic 27 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 27: Viral Hepatitis 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 common viral hepatitis (causative agents, transmission, signs and symptoms) • Describe treatment, prevention and control of viral hepatitisResources 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 viral | | | | |Hepatitis | |3 |15 minutes |Presentation |Signs and Symptoms of viral | | | | |Hepatitis | |4 |15 minutes |Presentation |Treatment, Prevention and Control | | | | |of viral Hepatitis | |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 Viral Hepatitis (15 minutes) • Hepatitis o Hepatitis is the inflammation of the liver, which may result from various causes, both infectious i.e. viral, bacterial, fungal, and parasitic organisms and non-infectious e.g. alcohol, drugs, autoimmune and metabolic diseases • Acute Viral Hepatitis o Acute viral hepatitis is a systemic infection predominantly affecting the liver caused by hepatotropic viral agents namely Hepatitis A virus (HAV), Hepatitis B virus (HBV), Hepatitis C virus (HCV), Hepatitis D virus (HDV), and Hepatitis E virus (HEV) o In most cases, acute viral hepatitis leads to a self-limiting disease but can take a fulminant course and lead to hepatic failure • Chronic viral hepatitis o This is a chronic inflammatory reaction that on going beyond 6monts from the acute infection. o Most common causative agents are HBV, HCV, and HDV which potentially leads to liver fibrosis, cirrhosis and portal hypertension, hepatocellular carcinoma and hepatic failure. • Transmission of hepatitis viruses o Hepatitis A virus (HAV) and hepatitis E virus (HEV) are transmitted by faecal-oral route through consumption of contaminated food or water o Hepatitis B virus (HBV) is transmitted through exposure to infective blood, semen, and other body fluids. HBV can be transmitted from infected mothers to infants at the time of birth or from family member to infant in early childhood. Transmission may also occur through transfusions of HBV-contaminated blood and blood products, contaminated injections during medical procedures, and through injection drug use o Hepatitis C virus (HCV) is mostly transmitted through exposure to infective blood. This may happen through transfusions of HCV- contaminated blood and blood products, contaminated injections during medical procedures, and through injection drug use. Sexual transmission is also possible, but is much less common. STEP 3: Signs and Symptoms of Viral Hepatitis (15 minutes) • Acute viral hepatitis o Fever, anorexia, malaise, jaundice and abdominal pain o Enlarged and tender liver o Altered consciousness, coma (hepatic encephalopathy), and bleeding stigmata (in fulminant cases) • Chronic viral hepatitis o Usually asymptomatic o Right upper quadrant abdominal pains o Fatigue, malaise, anorexia, low grade fever; jaundice is frequent in severe disease o Ascites, variceal bleeding, encephalopathy, coagulopathy, and hypersplenism o Urticarial, arthritis, vasculitis, polyneuropathy, glomerulonephritis, thyroiditis STEP 4: Treatment, Prevention and Control of Viral Hepatitis (15 minutes) Treatment of Acute Hepatitis • Acute Viral Hepatitis o There is no specific treatment to alter the course of acute viral hepatitis o Supportive management including hydration, feeding, control fever and pain if present is required. o Fulminant cases may require specific antiviral medications • Chronic Viral Hepatitis o Hepatits B Virus ▪ Tenofovir ▪ Entecavir ▪ Lamivudine o Hepatitis C Virus ▪ Ledpasvir ▪ Sufosvir ▪ Ribavirin • Prevention and control of viral hepatitis o Immunization o Personal and environmental hygiene o Safe sexual practices o Safe blood STEP 5: Key Points (5 minutes) • Hepatitis is the inflammation of the liver, which may result from various causes, both infectious i.e. viral, bacterial, fungal, and parasitic organisms and non-infectious e.g. alcohol, drugs, autoimmune and metabolic diseases • Viral hepatitis can be acute or chronic • Acute viral hepatitis is a systemic infection predominantly affecting the liver caused by hepatotropic viral agents namely Hepatitis A virus (HAV), Hepatitis B virus (HBV), Hepatitis C virus (HCV), Hepatitis D virus (HDV), and Hepatitis E virus (HEV) • Chronic hepatitis is most commonly caused by HBV, HCV, and HDV which potentially leads to liver fibrosis, cirrhosis and portal hypertension, hepatocellular carcinoma and hepatic failure. • Acute viral hepatitis is symptomatic while chronic viral hepatitis is usually asymptomatic • Treatment of viral hepatitis is supportive for acute hepatitis and involves use of antiviral drugs in chronic hepatitis STEP 6: Evaluation (5 minutes) • What is hepatitis? • How is viral hepatitis transmitted? • What are the treatment options for viral hepatitis? 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 ← Previous TopicNext Topic →View all Pharmaceutical Microbiology topicsOpen Complete Full Notes PDF / OFFLINE NOTES Unataka kutumiwa notes hizi kupitia WhatsApp?Kwa notes zilizopangiliwa vizuri kwa kusoma offline au PDF, bonyeza kitufe hapa chini. Ujumbe wenye Level, Semester, Module na Topic utaandaliwa moja kwa moja.TUMIWA NOTES WHATSAPP WhatsApp: 255620339260

NTA Level 5 • Semester 1 • PST05103 Rabies Pharmaceutical Microbiology • Source Session/Topic 28 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 28: Rabies 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: • List Describe rabies (causative agents, transmission, signs and symptoms) • To Describe treatment, prevention and control of rabies 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 Rabies | |3 |15 minutes |Presentation |Signs and Symptoms of Rabies | |4 |15 minutes |Presentation |Treatment and Prevention of Rabies| |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: Causes and Transmission of Rabies (15 minutes) • Rabies is an acute viral infection of the central nervous system that affects all mammal. • Rabies is caused by the Rabies virus infects the central nervous system, ultimately causing disease in the brain and death. • Rabies virus is a neurotropic virus that belongs to the genus lyssavirus of the family Rhabdoviridae o Rabies virus is a rod- or bullet-shaped, single-stranded, negative- sense, unsegmented, enveloped RNA virus • Rabies is transmitted to man by a bite wound from an infected animal via infected secretions, usually saliva. • Cycle o After inoculation, rabies virus may enter the peripheral nervous system directly and migrates to the brain or may replicate in muscle tissue, remaining sequestered at or near the entry site during incubation, prior to central nervous system invasion and replication. o It then spreads centrifugally to numerous other organs. [pic] STEP 3: Signs and Symptoms of Rabies (15 minutes) • Rabies infection has five general stages in humans: incubation, prodrome, acute neurologic period, coma, and death. o The incubation period is exceptionally variable, ranging from fewer than 10 days to longer than 2 years, but is usually 1–3 months. o Early or prodromal clinical features of the disease are non- specific and include ▪ Fever, general malaise and fatigue ▪ Respiratory system features (sore throat, cough, and dyspnea), ▪ gastrointestinal system features (anorexia, dysphagia, nausea, vomiting, abdominal pain, and diarrhea) ▪ Central nervous systems (headache, vertigo, anxiety, apprehension, irritability, and nervousness o The late features of the disease are: ▪ Excessive motor activity and agitation, confusion, hallucinations, excessive salivation, convulsions, priapism, increased libido, hydrophobia, insomnia, nightmares and depression • Death is considered as invariable outcome. STEP 3: Treatment, Prevention and Control of Rabies (15 minutes) • Treatment of rabies include; o Local wound therapy ▪ The bite wound is thoroughly washed with water and soap ▪ Then washed with 0% Povidone iodine to prevent secondary bacterial infection o To prevent or treat bacterial infection antibiotics are used; ▪ Amoxycillin with clavulanic acid ▪ Ciprofloxacin ▪ Clindamycin ▪ Trimothoprime/sulphamethoxazole o Passive immunization ▪ Anti-rabies human immunoglobulin • Parenterally and the other half injected into and around the wound o Active immunization ▪ Human Diploid Cell Vaccine (HDCV) ▪ Tetanus toxoid vaccine • Prevention and control o Animal rabies is prevented by vaccinating susceptible species, particularly dogs and cats. ▪ This reduces transmission to humans o Human rabies is best prevented by avoiding exposures to the disease ▪ If exposure occurs, postexposure prophylaxis is necessary and should be initiated promptly. ▪ Postexposure prophylaxis consists of the combination of local wound cleansing, human rabies immune globulin (HRIG) and rabies vaccine. STEP 4: Key Points (5 minutes) • Rabies is a fatal viral infection that attacks the central nervous and respiratory systems of mammals, including humans. • It is caused by a bite from an infected animal via secretions usually saliva. Human infection can be from rabid dogs, bats and other animals. • The disease attacks the central nervous system causing non-specific illness which later develop to severe neurological dysfunction and death • Rabies is best prevented than treated by avoiding exposure to the virus through vaccination of animals and in case exposure occurs immediate institution of post exposure prophylaxis. STEP 5: Evaluation (5 minutes) • How is rabies transmitted? • What are the preventive and control measures for rabies? • Name the medicines that are used in the management of rabies. 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 ← Previous TopicNext Topic →View all Pharmaceutical Microbiology topicsOpen Complete Full Notes PDF / OFFLINE NOTES Unataka kutumiwa notes hizi kupitia WhatsApp?Kwa notes zilizopangiliwa vizuri kwa kusoma offline au PDF, bonyeza kitufe hapa chini. Ujumbe wenye Level, Semester, Module na Topic utaandaliwa moja kwa moja.TUMIWA NOTES WHATSAPP WhatsApp: 255620339260

NTA Level 5 • Semester 1 • PST05103 Viral Haemorrhagic Fevers Pharmaceutical Microbiology • Source Session/Topic 29 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 29: Viral Haemorrhagic Fevers 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 Viral haemorrhagic fever (causative agents, transmission, signs and symptoms) • Describe treatment, prevention and control of Viral haemorrhagic fever 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 |Introduction to Haemorrhagic | | | | |Fevers | |3 |30 minutes |Presentation |Ebola Haemorrhagic Fever | |4 |15 minutes |Presentation |Marburg Haemorrhagic Fever | |5 |10 minutes |Presentation |Rift Valley Fevers | |6 |15 minutes |Presentation |Dengue Haemorrhagic Fever | |7 |10 minutes |Presentation |Yellow Fever | |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: Introduction to Haemorrhagic Fevers (25 minutes) • Viral haemorrhagic fevers (VHFs) are a group of illnesses caused by several distinct families of viruses • Common features of VHFs; o They affect many organs o They damage the blood vessels o They affect the body's ability to regulate itself o Some VHFs cause mild disease, but some, like Ebola or Marburg, cause severe disease and death • VHFs are caused by viruses of five distinct families; Arenaviridae, Bunyaviridae, Filoviridae, Flaviviridae, and Paramyxoviridae • These five families share the following features; o They are all RNA viruses, and are all covered, or enveloped, in a fatty (lipid) coating o Their survival is dependent on an animal or insect host, called the natural reservoir o Humans are not the natural reservoir for any of these viruses o Humans are infected when they come into contact with infected hosts ▪ However, with some viruses, after the accidental transmission from the host, humans can transmit the virus to one another o Human cases or outbreaks of haemorrhagic fevers caused by these viruses occur sporadically and irregularly; occurrence of outbreaks cannot be easily predicted o With a few noteworthy exceptions, there is no cure or established drug treatment for VHFs o The viruses are geographically restricted to the areas where their host species live ▪ Lassa fever is limited to rural areas of West Africa where rats and mice carry the virus STEP 3: Ebola Haemorrhagic Fever (30 minutes) • Cause and Transmission o Ebola is an acute viral infection caused by Ebolavirus, a filovirus that causes haemorrhage, multiple organ failure, and high mortality rates o Primary transmission is from animal to human, through contact with an infected animal or its product o Secondary transmission is from person to person through: ▪ Broken skin, mucous membrane or exchange of bodily fluids or ingestion, inhalation and injection of infectious material ▪ Breast feeding ▪ Sexual contact ▪ The disease can spread rapidly within the health care setting. • Signs and Symptoms o Incubation period is 2 to 20 days o High grade fever o Head ache o Body ache o Abdominal pain, nausea, vomiting and diarrhoea o Photophobia, conjunctival injection, jaundice, and lymphadenopathy o Upper respiratory symptoms (cough, chest pain, pharyngitis) o Haemorrhagic symptoms (unexplained bleeding) o CNS symptoms (Delirium, stupor, and coma) o A maculopapular rash, primarily on the trunk, begins around day 5 • Treatment and Prevention o Non-Pharmacological Treatment ▪ There is no specific treatment for Haemorrhagic Fever ▪ Supportive therapy includes • Mechanical ventilation, renal dialysis, and anti-seizure therapy may be required • Management of complications symptomatically • Maintaining Oxygen status and blood pressure o Pharmacological Treatment ▪ Paracetamol ▪ Treat for any complicating infection and co-morbid condition • B: ▪ Oxygen and management of hypoglycaemia if present ▪ Fluid and electrolyte balance • Sodium Lactate Compound (Ringers Lactate) • NS intravenously if patient cannot take fluids orally o Prevention ▪ Strictly isolation and handling of patients ▪ Wearing of completely body covering protective gears when handling patients ▪ Special and strictly handling of the dead STEP 4: Marburg Haemorrhagic Fever (15 minutes) • Cause and Transmission • Marburg is severe type of haemorrhagic fever which affects both animals and humans • It is caused by the Marburg virus and it is related to Ebola virus and a parent type belongs to viral haemorrhagic fevers of Filoviridae family • Transmission o Spread of the virus between humans has occurred in a setting of close contact, often in a hospital o Droplets of body fluids, or direct contact with persons, equipment, or other objects contaminated with infectious blood or tissues are all highly suspect as sources of disease o Transmission through infected semen can occur up to seven weeks after clinical recovery o Transmission does not occur during the incubation period • Signs and Symptoms o Incubation period is between 3-9 days o All age groups are susceptible but most case to adults o Signs and symptoms occur in two phases: ▪ Phase One • Sudden onset of fever, chills, headache and myalgia ▪ Phase Two • Maculopapular rashes, Trunk rash, Nausea, Vomiting, Sore throat, Abdominal pain, Diarrheal, Jaundice, Pancreas inflammation, Severe weight loss Liver failure, Massive haemorrhage (all orifices), Multi- organ dysfunction, Delirium, Shock, and Death • Treatment and Prevention o There is no specific treatment, cure, or vaccine for Marburg Haemorrhagic fever o Supportive hospital therapy: ▪ Fluid and Electrolyte balancing ▪ Oxygen ▪ Blood transfusion and clotting factors ▪ Treatment of complicating infections o Prevention ▪ Isolation of patients ▪ Wearing protective gears when attend patients or

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,