Pharmaceutical Sciences Notes

NTA Level 5 • Semester 1 • PST05103 Urinary Tract Infection and E-coli associated Diarrheal Pharmaceutical Microbiology • Source Session/Topic 20 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 20: Urinary Tract Infection and E-coli associated Diarrheal Diseases 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 Urinary Tract Infection and E-coli associated Diarrheal Diseases (causative agents, transmission, signs and symptoms) • Describe treatment, prevention and control of Urinary Tract Infection and E-coli associated Diarrheal 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 | 30 minutes|Presentation |Cause of Urinary Tract Infection | |3 | |Small group |Signs and Symptoms of Urinary | | |20 minutes |discussion/ |Tract Infection | | | |Presentation | | |4 |20 minutes |Presentation |Treatment, Prevention and Control | | | | |of Urinary Tract Infection | |5 |30 minutes |Presentation |E.coli associated Diarrheal | | | | |Diseases | |6 |10 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: Cause of Urinary Tract Infection (30 minutes) • Urinary tract infection (UTI) is the presence of an infection in the urinary tract. • Urinary tract infections (UTIs) can be divided into upper tract infections, which involve the kidneys (pyelonephritis) and lower tract infections, which involve the bladder (cystitis), urethra (urethritis) and prostate (prostatitis) • Urinary tract infection may be caused by fungi, viruses, and parasites • E. coli is the most common cause of urinary tract infection and accounts for approximately 90% of first urinary tract infections in young women • There are two types of UTI, complicated UTI and uncomplicated UTI • Uncomplicated UTI o Is usually considered to be cystitis or pyelonephritis that occurs in premenopausal adult women with no structural or functional abnormality of the urinary tract and who are not pregnant and have no significant comorbidity that could lead to more serious outcomes o In men, most UTIs occur in children or elderly patients, are due to anatomic abnormalities or instrumentation, and are considered complicated. • Complicated UTI o Occurs both in male and female following underlying cause such as structural or functional abnormality in the urinary tract, comorbidity, recent instrumentation or surgery of the urinary tract • Some risk factors for UTI include sexual intercourse, diaphragm and spermicide use, broad spectrum antibiotic use and new sex partner within the past year. STEP 3: Signs and Symptoms of Urinary Tract Infection (20 minutes) |Activity: Small Group Discussion (10 minutes) | | | |DIVIDE students into small manageable groups | | | |ASK students to discuss on the following; | |Write down the signs and symptoms of urinary tract infection (UTI) | | | |ALLOW students to discuss for 10 minutes | | | |ALLOW few groups to present and the rest to add points not | |mentioned | | | |CLARIFY and SUMMARIZE by using the contents below | • The symptoms and signs include o Urinary frequency o Dysuria o Hematuria o Pyuria o Flank pain/tenderness (associated with upper tract infection) o Fever of 38°C or higher o Tachypnoea, Tachycardia, Confusion and Hypotension o Vomiting STEP 4: Treatment, Prevention and Control of Urinary Tract Infection (20 minutes) • Non pharmacological management o Adequate hydration • Pharmacological management o Antibiotics ▪ Fluoroquinolones e.g. ciprofloxacin ▪ Penicillin e.g. amoxicillin/clavulanic acid ▪ Cephalosporins e.g. ceftriaxone ▪ Aminoglycosides e.g. gentamycin • Prevention and control of UTI involves; o Increasing fluid intake o Avoiding spermicides and diaphragm use o Not delaying urination o Wiping front to back after defecation o Avoiding douching o Urinating immediately after sexual intercourse STEP 5: E. coli associated Diarrhoeal Diseases (30 minutes) • E. coli that causes diarrhea are extremely common worldwide. • The E. coli are classified by the characteristics of their virulence properties and each group causes disease by a different mechanism • Enteropathogenic E coli (EPEC) o Enteropathogenic E. coli are an important cause of diarrhea in infants, especially in developing countries o EPEC adhere to the mucosal cells of the small bowel and cause lesions which result in diarrhoea o The result of EPEC infection in infants is characterized by severe, watery diarrhea, vomiting, and fever, which are usually self-limited but can be prolonged or chronic o The duration of the EPEC diarrhea can be shortened and the chronic diarrhea cured by antibiotic treatment • Enterotoxigenic E coli (ETEC) o Enterotoxigenic E coli (ETEC) are a common cause of “traveler’s diarrhea” and a very important cause of diarrhea in children less than 5 years of age in developing countries o ETEC produce enterotoxins and Shiga-like toxins that are identical to the Shiga toxin of Shigella dysenteriae • Enteroinvasive E coli (EIEC) o Enteroinvasive E. coli (EIEC) produce a disease very similar to shigellosis. o The disease occurs most commonly in children in developing countries and in travelers to these countries. o Similar to Shigella, EIEC strains are nonlactose or late lactose fermenters and are nonmotile o EIEC produce disease by invading intestinal mucosal epithelial cells • Enteroaggregative E coli (EAEC) o Enteroaggregative E. coli (EAEC) causes acute and chronic diarrhea (>14 days in duration) in persons in developing countries o These organisms also are the cause of foodborne illnesses in industrialized countries and have been associated with traveler’s diarrhea and persistent diarrhea in patients with HIV o They are characterized by their specific patterns of adherence to human cells • These diarrheal diseases are treated by fluids and

NTA Level 5 • Semester 1 • PST05103 Shigellosis, Enteric Fever and Peptic Ulcer Disease Pharmaceutical Microbiology • Source Session/Topic 21 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 21: Shigellosis, Enteric Fever and Peptic Ulcer Disease 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 Shigellosis, Enteric Fever and Peptic Ulcer Disease • (causative agents, transmission, signs and symptoms) Describe treatment, prevention and control of Shigellosis, Enteric Fever and Peptic Ulcer Disease 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 | 35 minutes|Presentation |Shigellosis | |3 |35 minutes |Brainstorming/|Typhoid Fever | | | |Presentation | | |4 |35 minutes |Brainstorming/|Peptic Ulcer Disease | | | |Presentation | | |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: Shigellosis (35 minutes) • Cause and Transmission o Shigellosis is an infectious disease caused by shigella (Shigella dysenteriae) o Most who are infected with shigella develop diarrhea, fever, and stomach cramps starting a day or two after they are exposed to the bacteria • Signs and Symptoms o Sudden onset of severe abdominal cramping, high-grade fever, emesis, anorexia, and large-volume watery diarrhea o Abdominal pain, tenesmus, urgency, fecal incontinence, and small volume of bloody, mucoid diarrhoea. o Extra intestinal manifestations associated with S. dysenteriae may include the following: ▪ Severe headache, lethargy, meningismus, delirium, and convulsions ▪ Hemolytic uremic syndrome (HUS), microangiopathic hemolytic anemia, thrombocytopenia, and renal failure, profound dehydration and hypoglycemia • Treatment o Replacement of fluids and electrolytes o Antibiotics ▪ Ciprofloxacin ▪ Nalidixic acid ▪ Erythromycin • Prevention and Control o Hygienic disposal of refuse o Hygienic food handling o Personal hygiene e.g. washing hands after using toilets and before eating o Washing of fruits and vegetables STEP 3: Typhoid Fever (35 minutes) • Cause and Transmission o Typhoid fever is also known as Enteric fever o Typhoid fever is an acute systemic disease caused by the gram- negative bacteria Salmonella typhi. o Salmonella paratyphi causes paratyphoid fever which has the same features as typhoid fever. o Typhoid infection is transmitted through ingestion of contaminated food and water • Signs and Symptoms |Activity: Brainstorming (5 minutes) | | | |Ask students to brainstorm on the following question: | | | |What are signs and symptoms observed in a patient with | |enteric fever? | | | |ALLOW few students to respond? | | | |WRITE their responses on the flip chart/ board | | | |CLARIFY and SUMMARIZE by using the content below | o The clinical manifestation and duration of illness vary markedly from one patient to another o The course of paratyphoid fever is shorter and less severe compared to that of typhoid fever o The major clinical features are: ▪ Fever, cramps, diarrhoea, severe headache, drowsiness and muscle pains (myalgia) ▪ Untreated, typhoid fever may progress to delirium, obtundation, intestinal hemorrhage, bowel perforation, and death ▪ Survivors may be left with long-term or permanent neuropsychiatric complications • Treatment Prevention and Control o Treatment ▪ Antibiotics • Fluoroquinolones e.g. Ciprofloxacin • Chloramphenicol o Prevention and control ▪ Washing hands after using toilets and before eating ▪ Food cleanliness ▪ Safe and hygienic food production STEP 4: Peptic Ulcer Disease (35 minutes) o Cause o Peptic ulcer disease is a circumscribed ulceration of the gastrointestinal mucosa occurring in areas exposed to acid and pepsin (lower oesophagus, stomach and duodenum) and most often caused by Helicobacter pylori infection o Gastro Esophageal Reflux Disease (GERD), a disorder resulting from gastric acid and other gastric contents into the esophagus due to incompetent barriers at the gastro esophageal junction may result in ulceration of the lower oesophagus • Signs and Symptoms o Peptic ulcer presents in many different ways o The commonest is chronic, episodic pain present in many different ways, and may persist for months or years. o However, the ulcer may come to attention as an acute episode with bleeding or perforation, with little or no previous history o Epigastric pain is the commonest symptom of peptic and gastric ulcer • Treatment Prevention and Control |Activity: Brainstorming (5 minutes) | | | |Ask students to brainstorm on the following question: | | | |What are the treatment options for Peptic Ulcer Disease? | | | |ALLOW few students to respond? | | | |WRITE their responses on the flip chart/ board | | | |CLARIFY and SUMMARIZE by using the content below | o Treatment goal for PUD ▪ To provide symptom relief and heal erosive esophagitis and prevent complication ▪ Anti secretory drugs and life style changes may be adequate if H. pylori is not present • H2 blockers e.g. Ranitidine • Proton Pump Inhibitors E.g. Omeprazole and Esomeprazole ▪ H. pylori is present in majority of PUD patients, therefore a triple therapy is used to eradicate the bacteria and provide relief and healing ▪ Generally, a combination of Proton Pump Inhibitor (PPI) + Amoxycillin or Azithromycin + Nitroimidazole is used. ▪ Recommended triple therapy for PUD are; • Omeprazole + Amoxicillin + Metronidazole • Lansoprazole + Azithromycin + Tinidazole • Prevention and Control o Discontinue NSAIDs and use paracetamol for pain control if possible o By using acid suppression e.g. Antacids o Smoking cessation o No dietary restrictions unless certain foods o Alcohol in moderation o Stress reduction STEP 5: Key Points (5 minutes) o Shigellosis is an infectious disease caused by Shigella dysenteriae o Most who are infected with

NTA Level 5 • Semester 1 • PST05103 Chlamydial Infections Pharmaceutical Microbiology • Source Session/Topic 22 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 22: Chlamydial 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 chlamydial infection (causative agents, transmission, signs and symptoms) • Describe treatment, prevention and control chlamydial infection 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 |Characteristics of Chlamydia | |3 |10 minutes |Presentation |Cause and Transmission of Trachoma| |4 |30 minutes |Presentation |Signs and Symptoms of trachoma | |5 |20 minutes |Presentation |Treatment, Prevention and Control | | | | |of trachoma | |6 | |Presentation |Non gonococcal urethritis and | | |30 minutes | |Lymphogranuloma Venereum | |7 |5 minutes |Presentation |Key Points | | 8|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: Characteristics of Chlamydia (15 minutes) • The genus chlamydia consists of obligate intracellular bacteria • The bacteria have cell wall resembling Gram negative bacteria but do not have peptidoglycan. They have DNA, RNA and ribosomes. • All chlamydiae exhibit similar morphologic features, share a common group antigen, and multiply in the cytoplasm of their host cells by a distinctive developmental cycle • The chlamydiae lack mechanisms for the production of metabolic energy and cannot synthesize adenosine triphosphate (ATP) • This restricts them to an intracellular existence, where the host cell furnishes energy-rich intermediates • Three species of Chlamydiae infect humans namely Chlamydia trachomatis, Chlamydia pneumoniae, and Chlamydia psittaci • C. trachomatis causes Trachoma, urogenital infections, lymphogranuloma venerium and pneumonia • C. pneumoniae causes bronchitis, sinusitis and pneumonia • C. psittaci causes psittacosis STEP 3: Cause and Transmission of Trachoma (10 minutes) • Trachoma is a chronic conjunctivitis caused by infection with Chlamydia trachomatis • It is one of the commonest causes of blindness worldwide. • It is a chronic keratoconjunctivitis that begins with acute inflammatory changes in the conjunctiva and cornea and progresses to scarring and blindness • The disease is associated with poverty and crowded living conditions • It is endemic in Africa, middle east, India and South East Asia, mostly affecting children • Trachoma is transmitted through inoculation of eye by contaminated hands, flies, clothing and droplets. STEP 4: Signs and Symptoms of Trachoma (30 minutes) • The incubation period for chlamydial conjunctival infection is 3–10 days • In endemic areas, initial infection occurs in early childhood, and the onset of the long-term consequence, trachoma, is insidious • Chlamydial infection is often mixed with bacterial conjunctivitis in endemic areas, and the two together produce the clinical picture • The earliest features of trachoma are lacrimation, mucopurulent discharge, conjunctival hyperemia, and follicular hypertrophy • Microscopic examination of the cornea reveals epithelial keratitis, subepithelial infiltrates, and extension of limbal vessels into the cornea (pannus) • As the pannus extends downward across the cornea, there are scarring of the conjunctiva, eyelid deformities (entropion, trichiasis), and an added insult caused by eyelashes sweeping across the cornea (trichiasis) • With secondary bacterial infection, loss of vision progresses over a period of years. • Generally, the signs and symptoms include; o Photophobia in early stages or re- infection o Follicles in the upper tarsal plate seen as round and white nodules in active diagnostic o In late stages, in-turned eyelashes rub on the cornea leading to corneal ulcers o Loss of vision due to corneal Scarring • Clinical Stages according to World Health Organization o Trachomatous Inflammation Follicular (TF) – Presence of at least 5 follicles on the upper tarsal plate o Trachomatous Inflammation Intense (TI) – There is intense inflammation, the conjunctival blood vessels cannot be seen o Trachomatous Scarring (TS) – Presence of white scars in the upper tarsal plate o Trachomatous Trichiasis (TT) – Presence of some eye lashes rubbing against the cornea o Corneal Opacity (CO) – Presence of corneal opacity (scar) affecting the central cornea STEP 5: Treatment, Prevention and Control of Trachoma (20 minutes) Treatment • Non pharmacological management o Face washing and total body hygiene to prevent transmission of disease from one person to the other o Environmental improvement/hygiene • Pharmacological management o Use of antibiotics ▪ Tetracyclines e.g. oxytetracycline ointment 3% ▪ Macrolides e.g. azithromycin • Surgery o To correct entropion in Trachomatous Trichiasis (TT) patients o This procedure can be done at a Dispensary or Health Centre and community level by a trained health worker Prevention and Control • The World Health Organization has initiated the S-A-F-E program to eliminate blinding trachoma and at least markedly reduce clinically active disease o Surgery for deformed eyelids o Antibiotic use involving periodic azithromycin therapy o Face washing and hygiene o Environmental improvement such as building latrines and decreasing the number of flies that feed on conjunctival exudates. STEP 6: Nongonococcal Urethritis and Lymphogranuloma Venereum (30 minutes) Urogenital infections • C. trachomatis also causes urogenital infections in both male and female • In female the infection is almost asymptomatic o May cause cervicitis, urethritis, salpingitis and postpartum fever • In male the infection is symptomatic o It causes nongonococcal urethritis (which must be ruled out in treatment of gonorrhea or co-treated) o Urethritis, dysuria and pyuria o It is a common cause of post-gonococcal urethritis • Treatment options include use of Tetracycline e.g. doxycycline, macrolides e.g. erythromycin and sulphonamides • Preventive measures include sanitation, safe sex practices, treatment of patients and their sexual partners. Lymphogranuloma venereum (LGV) • Is a sexually transmitted infection caused

NTA Level 5 • Semester 1 • PST05103 Spirochetes Infection Pharmaceutical Microbiology • Source Session/Topic 23 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 23: Spirochetes Infection 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 bacterial diseases (causative agents, transmission, signs and symptoms) • Describe treatment, prevention and control of common bacterial 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 | 10 minutes|Presentation |Characteristics of Spirochetes | |3 |5 minutes |Presentation |Cause and Transmission of Syphilis| |4 | |Small group |Signs and Symptoms of Syphilis | | |20 minutes |discussion/ | | | | |Presentation | | |5 |10 minutes |Presentation |Treatment, Prevention and Control | | | | |of Syphilis | |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: Characteristics of Spirochetes (10 minutes) • Spirochetes are a large, heterogeneous group of spiral, motile bacteria • One family (Spirochaetaceae) of the order Spirochaetales consists of two genera whose members are human pathogens, Borrelia and Treponema • Spirochetes are long, slender, helically coiled, spiral, or corkscrew- shaped bacilli that are motile by endofagella or internal flagella • Spirochaetes are distinguished from other bacterial phyla by the location of their flagella (sometimes called axial filaments or endofagella or internal flagella) which run lengthwise between the bacterial inner membrane and outer membrane in periplasmic space • Spirochetes are susceptible to drying and chemicals o They are readily killed in dry conditions and various chemical agents including penicillins. • The spirochetes are so thin that they are not readily seen unless immunofluorescent stain or dark-field illumination is used • Treponema pallidum is a spirochete bacterium with subspecies that cause treponemal diseases such as syphilis, bejel, pinta, and yaws. STEP 3: Cause and Transmission of Syphilis (5 minutes) • Syphilis is a sexually transmitted spirachetal infection characterized by one or more skin lesions (chancres) at the site where the spirochete penetrated • Syphilis is caused by the bacterium Treponema pallidum subspecies pallidum • Syphilis is transmitted through sexual intercourse with an infected person, close contact with active lesions, blood transfusion and passage to placenta in pregnancy (congenital syphilis) STEP 4: Signs and Symptoms of Bacillus Food Poisoning (20 minutes) |Activity: Small Group Discussion (10 minutes) | | | |DIVIDE students into small manageable groups | | | |ASK students to discuss on the following question | |What are the clinical manifestations of syphilis? | | | |ALLOW students to discuss for 15 minutes | | | |ALLOW few groups to present and the rest to add points not | |mentioned | | | |CLARIFY and SUMMARIZE by using the contents below | • Incubation period is 3 to 90 days • Early or primary syphilis o General lymphadenopathy ▪ Lymph node enlarges and become rubbery, painless, discrete and mobile o One or more skin lesion ▪ A papule develops at site of entry and breaks down to form an ulcer with clean base “a chancre” o This primary lesion heals spontaneously and later reappear • Secondary syphilis o Signs of disseminated disease appear, with prominent skin lesions dispersed over the entire body surface. ▪ Rash on trunc and promal extremeties spreading to involve palms and soles ▪ Fever, malaise, headache o Spontaneous remission may occur after the primary or secondary stages or the disease may progress to the late phase (tertiary syphilis) • Tertiary syphilis o Manifest years after chancres have healed o Virtually all tissues may be involved ▪ Cardiovascular syphilis, neurosyphilis • Latent syphilis shows no symptoms • Congenital syphilis o In utero infections can lead to serious fetal disease, resulting in latent infections, multiorgan malformations, or death of the fetus o Most infected infants are born without clinical evidence of the disease, but rhinitis then develops and is followed by a widespread desquamating maculopapular rash o Teeth and bone malformation, blindness, deafness, and cardiovascular syphilis are common in untreated infants who survive the initial phase of disease STEP 5: Treatment, Prevention and Control of Syphilis (10 minutes) • Treatment options o Antibiotics ▪ Penicillins • Benzathine Penicilli • Benzyl penicillin ▪ Macrolides • Azithromycin ▪ Tetracyclines • Doxycycline • Preventive and control measures o Early diagnosis and treatment o Safe sex practices e.g. use of condoms o Detection and treatment of pregnant STEP 6: Key Points (5 minutes) • Spirochetes are a large, heterogeneous group of spiral, bacteria that move by endogeonous flagella • Treponema pallidum is a spirochete bacterium with subspecies that cause treponemal diseases such as syphilis, bejel, pinta, and yaws. • Treponema pallidum subspecies pallidum causes syphilis in humans. • Syphilis is a sexually transmitted infection which is characterized by painless chancre and progression to chronic disease • Syphilis is treated by antibiotics such as penicillins and prevented by safe sex practices and early diagnosis and treatment of patient to prevent progression of the disease. STEP 7: Evaluation (5 minutes) • What is a chancre? • How is syphilis transmitted? • What are the medicines used for treatment of syphilis? 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

NTA Level 5 • Semester 1 • PST05103 Introduction Virus Pharmaceutical Microbiology • Source Session/Topic 24 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 24: Introduction Virus 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 virology • Describe general structure and properties of viruses • Classify viruses according to their genetic and morphological properties • Describe viral-host-cell interaction and replication • List various drug targets in virus 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 | |Presentation |Common terms used in Virology | | |10 minutes | | | |3 |10 minutes |Buzzing/ |Characteristics of viruses | | | |Presentation | | |4 |25 minutes |Presentation |Viral structure | |5 |30 minutes |Presentation |Classification of viruses | |6 |15 minutes |Presentation |Viral-host cell interaction and | | | | |replication | |7 |15 minutes |Presentation |Drug targets in viruses | |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 Terms Used in Virology (10 minutes) • Virology o Virology is the study of viruses. Their structures and activities including infections caused by viruses. • Virus o This is a very small acellular particle that can only replicate inside cells of another organism. A virus is capable of infecting cells and potentially cause disease • Virion o Is complete virus particle. • Capsid o Is the protein shell or coat that encloses the nucleic acid of a virus • Capsomeres o Morphological units seen in electron microscopes that make up the capsid • Envelope o A lipid-containing membrane that surrounds some viruses. It is acquired during maturation by a budding process through the cell membrane. • Peplomers o Are virus-encoded glycoproteins that are exposed on the surface f the envelope • Nucleocapsid o This is the protein-nucleic acid complex representing the packed form of the viral genome. STEP 3: Characteristics of Viruses (10 minutes) |Activity: Buzzing (5 minutes) | | | |ASK students to pair up and buzz on the following question for 2 | |minutes | | | |What are the characteristics of viruses? | | | |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 | • Characteristics of viruses include; o They infect prokaryotic and eukaryotic cells o They are acellular o They contain either DNA or RNA surrounded by a protein coat o Viruses are obligate intracellular entities o They cannot reproduce outside a host cell ▪ Viruses are cultivated in living cells e.g. bacteria ▪ Viruses that infect bacteria are called bacteriophage ▪ Some viruses multiply in cytoplasm of host cell while others multiply in the nucleus of host cells o They are very small (the largest virus is the size of a small bacteria) o Some viruses have envelope outside the capsid while other are naked STEP 4: Viral Structure (25 minutes) • A complete viral particle (virion) consists of; o Nucleic acid ▪ A virus contains only one type of nucleic acid (DNA or RNA) that can be linear or circular, segmented or one molecule. • The viral DNA o single-stranded DNA (ssDNA) o double-stranded DNA (dsDNA) o single-stranded RNA (ssRNA) ▪ The RNA can be of positive sense (+) which is the same as Mrna or a negative sense (-) which is complementary to mRNA • double-stranded RNA (dsRNA) o Protein coat (capsid): ▪ The nucleic acid is surrounded by a protein coat (the capsid) ▪ The capsid is formed from protomers which collectively form capsomeres. The capsomere is the basic unit of the capsid ▪ The capsid protects the virion in the external environment ▪ It also helps in transfer of nucleic acid between host cells ▪ The capsid and the nucleic acid are collectively called Nucleocapsid ▪ Viral Symmetry • Capsid is constructed in a highly symmetrical manner o Icosahedral ▪ The capsid is composed of triangular faces made from capsomeres (hexons) ▪ The virus appears spherical e.g. poliovirus o Helical ▪ Virus is hollow, cylindrical in shape ▪ The virus can be rigid or flexible e.g. tobacco mosaic virus (TMV) o Complex ▪ Contains several types of symmetry in one virus o Viral envelope ▪ Some viruses have a lipid layer (the envelope) surrounding the nucleocapsid ▪ Viruses with the envelope are called enveloped viruses while those not containing the envelope are called non enveloped (or naked) virues ▪ Contains proteins projecting from the envelope. These proteins help with attachment of the virus to the host cells STEP 5: Classification of Viruses (30 minutes) • Viruses are not included in the five kingdom classification • Universal classification of viruses group viruses into orders, families, sub families, genera and species. • More than 24 families cause disease in human) • The nomenclature and classification of viruses do not use the conventional taxonomic groups o Suffix endings ▪ Genus –ends in ‘virus’ e.g. coronavirus ▪ Sub-family –ends in ‘virinae’ ▪ Family –ends in ‘viridae’ ▪ Order –ends in ‘virales’ ▪ Species –contains name of host, the word virus etc. • Viruses are classified based on the following criteria; o Nucleic acid type: DNA viruses and RNA viruses o Nature of the nucleic acid: linear, circular, segmented, non- segmented genome or polarity i.e. positive sense or negative sense of the

NTA Level 5 • Semester 1 • PST05103 Herpes Virus Infections Pharmaceutical Microbiology • Source Session/Topic 25 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 25: Herpes Virus 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 common viral diseases (causative agents, transmission, signs and symptoms) • Describe treatment, prevention and control of common viral 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 |25 minutes |Presentation |Characteristics of Herpes viruses | |3 |30 minutes |Presentation |Herpes Simplex Infections | |4 |30 minutes |Presentation |Varicella (Chickenpox) | |5 |20 minutes |Presentation |Herpes Zosters (Shingles) | |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: Characteristics of Herpes Viruses (25 minutes) • Herpes viruses belong to the family Herpesviridae • They are a group of virus that are widely spread in human population • They are among the leading cause of human viral diseases • They can cause overt disease or remain silent for many years, then reactivated • These viruses contain double-stranded DNA which is located at the central core • All herpesviruses establish latent infection within tissues that are characteristic for each virus, reflecting the unique tissue trophism of each member of this family • There are over one hundred viruses in the family but only eight are pathogenic to humans. These are known as human herpes viruses and they are; o Herpes Simplex Virus -1 –causes oral herpes o Herpes Simplex Virus -2 –causes genital herpes o Varicella zoster virus (VZV) –causes chickenpox and herpes zosters o Cytomegalovirus (CMV) –causes cytomegalovirus retinitis o Epstein-Barr virus (EBV) –causes infectious mononucleosis o Hhuman herpesvirus 6 (HH6) o Human herpesvirus 7 (HH7) o Human herpes virus 8/Kaposi's Sarcoma virus causes cancers • Members of herpes viruses are grouped into three subfamilies namely alpha herpesviruses, beta herpesviruses and gamma herpesviruses • After initial infection, all herpesviruses remain latent within specific host cells and may subsequently reactivate • Antiviral drugs that have activity against herpesviruses include acyclovir, cidofovir, famciclovir, fomivirsen, foscarnet, ganciclovir, idoxuridine, penciclovir, trifluridine, valacyclovir, valganciclovir, and vidarabine STEP 3: Herpes Simplex Virus Infections (30 minutes) Cause, Transmission and Manifestations • Herpes simplex viruses (HSV-1 and HSV-2) commonly cause recurrent infection affecting the skin, mouth, lips, eyes, and genitals • Common severe infections include encephalitis, meningitis, neonatal herpes, and, in immunocompromised patients, disseminated infection • Both types of herpes simplex virus (HSV), HSV-1 and HSV-2, can cause oral or genital infection • Most often, HSV-1 causes gingivostomatitis, herpes labialis, and herpes keratitis • HSV-2 usually causes genital lesions • Transmission of HSV results from close contact with a person who is actively shedding virus o HSV -1 is transmitted by respiratory droplets or direct contact with infected saliva and the infection usually limited to Oropharynx o HSV -2 is transmitted through sexual contact and from maternal genital infections to newborn during delivery or in utero • Viral shedding occurs from lesions but can occur even when lesions are not apparent. • After the initial infection, HSV remains dormant in nerve ganglia, from which it can periodically emerge, causing symptoms • Recurrent herpetic eruptions are precipitated by overexposure to sunlight, febrile illnesses, physical or emotional stress, immunosuppression and some unknown stimuli • Generally, HSV infection presents with the following signs and symptoms o Preceding tingling sensation, discomfort and itching o Grouped vesicles forming on the skin, and mucous membranes, particularly the buccal area, gentalia, conjunctivae, and cornea Treatment and Prevention • Antiviral drugs o Acyclovir o Valacyclovir o Famciclovir • Prevention o Hygiene o Treatment of mothers o Safe sex practices STEP 4: Varicella (Chickenpox) (30 minutes) • Chickenpox is an acute, systemic, usually childhood infection caused by the varicella-zoster virus (VZV) • Chickenpox is an acute invasive phase of the infection with VZV which lies dormant and reactivate later in life to cause shingles • It usually begins with mild constitutional symptoms that are followed shortly by skin lesions appearing in crops and characterized by macules, papules, vesicles, and crusting • Patients at risk of severe neurologic or other systemic complications (e.g. pneumonia) include adults, neonates, and patients who are immunocompromised or have certain underlying medical conditions • In immunocompetent children, chickenpox is rarely severe but in adults and immunocompromised children, infection can be serious • Generally, chickenpox presents with the following signs and symptoms o Red macular rash with a central vesicle (blister) on the trunk, oral mucosa and scalp o Pustules and crusting o Intense pruritus o Fever o Occasional regional lymphadenopathy • Treatment options for chickenpox include; o Antiviral drugs e.g. acyclovir o Antipyretic/analgesic e.g. Paracetamol o Antipruritic agent i.e. Calamine lotion with phenol STEP 5: Herpes Zosters (Shingles) (20 minutes) • Herpes zosters is an infection due to resurgence or reactivation of the Varicella zoster virus (VZV) which also causes chickenpox • Signs and Symptoms of Herpes zosters o Severe burning pain o Grouped vesicles overlying erythematous skin following a dermatomal distribution o Typically, lesions do not cross the midline • Treatment options o Antiviral drugs e.g. acyclovir o Antiseptics for the wounds e.g. Potassium permanganate 1:4000 solution o Antibiotics for secondary bacterial infections ▪ Topical gentamycin ▪ Mupirocin STEP 6: Key Points (5 minutes) • Herpes is a group of over hundred viruses that belong to family herpesviridae • Eight of the herpes are pathogenic to humans and they cause an initial illness then lie dormant in

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