2 A. DISEASES CAUSED THROUGH FECAL-ORAL ROUTE CLASS.pdf

18 July 2024 1 DISEASES CAUSED THROUGH THE FECAL ORAL ROUTE. BLOCK II 18 July 2024 2 AMOEBIASIS  18 July 2024 3 Objectives By the end of the lesson student...

18 July 2024 1 DISEASES CAUSED THROUGH THE FECAL ORAL ROUTE. BLOCK II 18 July 2024 2 AMOEBIASIS  18 July 2024 3 Objectives By the end of the lesson students will be able to; 1. Define amoebic dysentery 2. Outline the modes of transmission of amoebic dysentery 3. State the clinical manifestations of amoebic dysentery 4. Describe the pathophysiology of amoebic dysentery 5. Appreciate the medical management of amoebic dysentery 18 July 2024 4 AMOEBIC DYSENTERY. Definition It is a protozoan intestinal infection that is accompanied by extra intestinal features It is a worldwide disease that is endemic in most regions of the world 18 July 2024 5 Cont. Epidemics are only associated with poor water supply The infection may be asymptomatic or symptomatic Asymptomatic infection results in chronic carrier state for many years 18 July 2024 6 Epidemiology Ameobiasis is caused by protozoa called Entamoeba histolytica The incubation period is about 3-4 weeks. However if the infection is massive, the incubation period may be as short as few hours Humans are the only known reservoirs Susceptibility is universal 18 July 2024 7 Cont. The disease is communicable so as long as the cysts are being passed out in the feaces of the cases and carriers Modes of transmission Fecal oral route Vehicles are: contaminated food, fluids, fingers, fomites, and flies  18 July 2024 8 Pathophysiology The cysts are ingested through fecal oral route. They cysts escape destruction by the HCL in the stomach and proceed to the small intestines In the small intestines, the cysts change to trophozoites and are harmless commensals. However when the trophozoites get into the large intestines they become pathological  They attach to the mucosa of the colon, multiply and secrete enzyme proteases which erode the lining of the colon 18 July 2024 9 Cont. The erosion results in intestinal ulceration and formation of pus pockets The pus pockets gradually develop into intestinal abscesses Repeated infection causes scaring of the muscular layer hence formation of a large hard swelling called Amoeboma. (A palpable mass that is often confused with a tumor)  18 July 2024 10  If the entire wall of the colon is perforated, peritonitis and extra intestinal abscesses result  In the course of ulceration, some trophozoites gain access to circulation and spread to the liver, lungs, brain, etc.. forming abscesses  In the large intestines, some trophozoites undergo encystment and are passed out in the stool and can infect another person 18 July 2024 11 18 July 2024 12 Pathophysiology of E. Hystolytica 18 July 2024 13 Amoebiasis 18 July 2024 14 Cysts and trophozoites 18 July 2024 15 Clinical Features  Diarrhea which may be mild or profuse and may gradually progress to become bloody and mucoid  Diarrhea may alternate with constipation  Abdominal pain which may be mild discomfort or severe colic abdominal pain  Abdominal tenderness  Low grade fever 18 July 2024 16 Headache Anorexia Nausea Weight loss Amoeboma: hard abdominal swelling felt on palpation 18 July 2024 17 Diagnosis Health history Physical examination Stool for cysts or trophozoites Ultrasound /CT scan  18 July 2024 18 Management Asymptomatic patients do not require treatment since they clear the infection with time Metronidazole 1.4g daily for 3 days for invasive cases Or Metronidazole 800mg three times daily for 5 days orally Tinidazole 2gm daily for 3 days 18 July 2024 19 Treatment continued…  Diloxanide furoate 500mg three times a day for 10 days  Emetine injection for 5 days  Incision and drainage of abscesses Metronidazole is the drug of choice for hepatic cases Large liver abscesses may need aspiration in hospital by a an experienced clinician  18 July 2024 20 Complications Amoebic liver abscess Intestinal perforation Acute peritonitis Amoebic Lung abscess Brain abscess Pleurisy. Empyema. Amoebic skin ulcers especially around the perianal area and surgical incision following incision and drainag 18 July 2024 21 Prevention and control Proper food handling Proper cooking of food Adequate treatment of cases Personal hygiene practices Hygienic kitchen practices Environmental hygiene  18 July 2024 22 Proper disposal of human excreta Clearing flying using insecticides Protecting water sources Proper refuse disposal Adequate sewage treatment Disinfection of contaminated articles and linen Screening food handlers 6 monthly Health education of the public on the disease and its preventive measures 18 July 2024 23 CHOLERA 18 July 2024 24 Objectives. By the end of the class the student should be able to; 1. Define cholera 2. State the causative organism of cholera 3. Outline the clinical features of cholera 4. Appreciate the pathophysiology of cholera 18 July 2024 25 Definition An acute bacterial intestinal disease characterized by sudden onset of profuse painless watery stools, nausea and profuse vomiting, rapid dehydration and circulatory collapse 18 July 2024 26 children are more susceptible It is common in lowest socioeconomic groups e.g. people in informal settlements Case fatality rate of untreated severe cholera exceeds 50% This can be reduced to below 1% by prompt management 18 July 2024 27 Etiology Cholera is caused by curved, motile, gram negative bacteria called vibrio cholerae There are four sub strains namely: 1. Eltor 2. Ogawa 3. Luaba 4. Hikojima 18 July 2024 28 Epidemiology The Eltor substrain is responsible for Cholera epidemics/pandemics The source of infection is feces and vomitus of infected persons or carriers Humans are the main reservoirs  18 July 2024 29 Incubation period is from a few hours to 5 days with an average of 2-3 days It is communicable so long as the vibrio are being excreted by the cases and carriers Vibrio cholera is very sensitive to gastric acid and so a large number of organisms must be ingested for the infection to occur  18 July 2024 30 After recovery from acute illness, the patient may become a convalescent carrier for a few weeks to several months Susceptibility is universal but risk is high in children 18 July 2024 31 Modes of transmission Fecal-oral route  Fingers, The vehicles are:  Fomites  Flies. contaminated food,  Another possible vehicle is fluids, inadequately cooked sea food  18 July 2024 32 Pathophysiology The vibrio gain access to the GIT through fecal oral route. Some are destroyed by HCL in the stomach while some pass on to the small intestines They rapidly multiply in the small intestines initiating inflammation of the intestinal mucosa 18 July 2024 33 Pathophysiology The inflammation is characterized by edema, secretion of mucus, fluid and electrolytes into the intestinal lumen and increased intestinal movements This produces the typical clinical features to include profuse diarrhea and vomiting 18 July 2024 34 Pathophysiology The infection is localized to the gut and does not gain access to the circulation The patient develops rapid dehydration, acidosis and circulatory collapse if not promptly managed as result of profuse diarrhea and vomiting 18 July 2024 35 Pathogenesis 18 July 2024 36 18 July 2024 37 Clinical features Profuse watery stools; Initially there is fecal matter which decreases rapidly to clear fluid with flakes of mucus giving it the classical rice-water stool appearance Profuse vomiting- initially with food particles but soon after only clear rice-water vomitus 18 July 2024 38 Clinical features Severe dehydration characterized by; Weak and rapid pulse Cold, dry and inelastic skin Decreased urine output Low blood pressure Sunken eye sockets Muscle cramps due to marked electrolyte imbalance. 18 July 2024 39 Diagnosis History Physical examination to confirm clinical features Stool/vomitus/rectal swab for microscopy to isolate the vibrio cholera 18 July 2024 40 Management Mild cases are self-limiting Severe cases require aggressive management In case of outbreaks, temporary treatment centers are created to manage the patient 18 July 2024 41 Management Management includes; Bed rest and isolation. Preferably nurse in a cholera bed Maintain clear airway by clearing the vomitus and placing patient in proper position to prevent aspiration of vomitus 18 July 2024 42 Management Fluid therapy both oral and intravenous Oral rehydration solutions are given as much as the patient is able to take or through a nasogastric tube Vomiting is not a contraindication for oral fluids. ½ strength Darrow's/ normal saline etc are appropriate for intravenous infusions 18 July 2024 43 Management Observations Vital signs 4 hourly Monitor for signs of dehydration Monitor for signs of shock Note frequency and character of vomitus/ stools  18 July 2024 44 Drugs Tetracycline is the drug of choice inadults: dosage is 500mg QID for 5-7 days Doxycycline may also be used: dosage is 100mg BD for 5-7 days or a single dose of 300mg Other alternative antimicrobials are septrin, erythromycin, and ciprofloxacin Dug of choice in children below 8years is erythromycin and cotrimoxazole (Find out why tetracycline cannot be used in these group)  18 July 2024 45 Diet-balanced Maintain ORS in acute phase, then to fluid diet and graduate to normal diet gradually  The meals should be in small but frequent amounts  18 July 2024 46 Infection prevention Includes hand washing, gloving and disinfection of contaminated articles, equipment's, and linen Assist with ADL – both hygiene and elimination. Note the urine output and monitor the number and character of stools. Psychological care  18 July 2024 47 Health education and discharge on; Disease and preventive measures Diet Drug compliance 18 July 2024 48 Complications Metabolic acidosis Hypovolemic shock Acute renal failure 18 July 2024 49 Prevention and control Adequate treatment of cases Isolation of acute cases Tetracycline 2 gram stat as chemoprophylaxis for contacts and health care personnel. Oral Cholera vaccine in presence of outbreaks. Gives protection for a few months 18 July 2024 50 Prevention and control Personal hygiene practices especially hand washing Hygienic kitchen practices such as covering food, boiling drinking water, washing fruits and vegetables etc 18 July 2024 51 Prevention and control Environmental hygiene- proper disposal of human excreta, proper disposal of refuse, safe sanitation. Closing public eating places and open air markets during the outbreak Disinfection of articles & linen contaminated with feaces and vomitus of infected persons. 18 July 2024 52 Prevention and control Notification of cases locally and internationally. Screening of food handlers 6 monthly. Public health education. Diseases surveillance. 18 July 2024 53 Prevention and control Environmental hygiene- proper disposal of human excreta, proper disposal of refuse, safe sanitation. Closing public eating places and open air markets during the outbreak Disinfection of articles & linen contaminated with feaces and vomitus of infected persons. 18 July 2024 54 Prevention and control Notification of cases locally and internationally Screening of food handlers 6 monthly Public health education Diseases surveillance. 18 July 2024 55. BACILLARY DYSENTERY (shigellosis) 18 July 2024 56 Objectives By the end of the lesson the learner will be able to; 1. Define bacillary dysentery 2. Outline the clinical picture of bacillary dysentery 3. Distinguish between bacillary and amoebic dysentery 4. Describe the management of bacillary dysentery 5. Explain the prevention and control measures of bacillary dysentery  18 July 2024 57 BACILLARY DYSENTERY Definition Dysentery: this is the passing of bloody mucoid stools accompanied by abdominal pain with or without tenesmus(Rectal tenesmus – a clinical symptom, where there is a feeling of constantly needing to pass stools, despite an empty colon) Bacillary dysentery is an acute bacterial intestinal disease characterized by bloody stools, fever, vomiting, abdominal cramps and tenesmus 18 July 2024 58 Bacillary dysentery It has a worldwide distribution but its particularly common throughout Africa It is more common in children than in adults, and common in the rainy season It is endemic in many parts of the world 18 July 2024 59 BACILLARY DYSENTERY Outbreaks are common in institutions such as prisons, mental hospitals, slums, refugee camps, orphanages and schools due to overcrowding and poor hygiene  18 July 2024 60 Pre-disposing factors. Improper disposal of faeces Lack of clean water especially if contaminated with fecal material High housefly population Floods with heavy contamination of water Malnutrition which lowers resistance to diseases Poor personal hygiene Poor and overcrowded living conditions 18 July 2024 61 Epidemiology Bacillary dysentery is caused by non-motile, gram negative bacteria of shigella species namely: S. sonnei S. flexneri S. dysenteriae S. boydii The first three are responsible for the outbreaks of dysentery S. boydii is responsible for sporadic cases of dysentery 18 July 2024 62 Epidemiology Humans are the only reservoirs The source of the infection is faeces of an infected person Incubation period is 1-4 days It is communicable during the acute infection and as long as the bacilli is excreted in the faeces  18 July 2024 63 The infection may be mild, asymptomatic and self limiting Asymptomatic infection may result in asymptomatic carrier state for a few months (for about three months) Following the acute infection, the person may become a convalescent carrier for about 4 weeks Adequate treatment shortens the carrier state  18 July 2024 64 Epidemiology Susceptibility is general but the disease is more severe in children Modes of transmission. Fecal-oral route. The vehicles are contaminated food, fluids, formites, fingers and flies 18 July 2024 65 Pathophysiology Bacilli gains entry to the GIT through the fecal- oral route. Some are destroyed by gastric acid while others pass on to the small intestines In the small intestines and colon, the bacilli multiply and produce enterotoxins triggering an intense inflammatory process  18 July 2024 66 Pathophysiology The inflammation causes secretion of water, mucous and electrolytes into the lumen of the intestines The mucosa is ulcerated and bleeds and hence bloody mucoid stools The inflammation also causes increased peristalsis hence increased bowel movements and diarrhea 18 July 2024 67 Pathophysiology The infection may be mild and self limiting especially in well nourished adults It may be acute, toxic and fatal especially in children, malnourished and immunosuppressed The toxins may gain access to circulation hence toxemia  18 July 2024 68 Clinical features 1. Mucoid bloody diarrhea initially has fecal matter which decreases as the disease progresses to contain only blood and mucus 2. Patient may have up to 20 motions in 24 hours 3. High fever which may produce convulsions in children 4. Colicky abdominal cramps 5. Nausea and vomiting 18 July 2024 69 Clinical features 6. Tenesmus – painful contractions of the anal sphincter producing an almost continuous and irresistible urge to defecate. However no faecal matter is produced. Only small quantities of purulent mucus and blood 7. Rapid pulse rate  18 July 2024 70 Clinical manifestations 8. Muscular cramps due to electrolyte imbalance 9. Signs of dehydration such as oliguria, low blood pressure, cold, dry, inelastic skin 10. Rectal prolapse in infants 18 July 2024 71 Diagnosis 1. History 2. Physical examination 3. Stool/ rectal swab for microscopy or culture to isolate the shigella 4. Full hemogram which reveals elevated WBC count  18 July 2024 72 Management 1. Bed rest and isolation in acute stage 2. Fluid therapy with oral rehydration solutions and intravenous fluids 3. Observations: Vital signs 4 hourly Signs of dehydration Character and frequency of stools  18 July 2024 73 Management. 4. Drugs: Antibiotics: appropriate as per culture and sensitivity results. This may be tetracycline, ampicillin, septrin, ampiclox, cephalosporins as prescribed; given for 7 days Spasmolytics such as belladonna and buscopan. Narcotics may be given in severe muscle cramps and tenesmus but not indicated  18 July 2024 74 Management. 5. Diet – after acute phase, introduce light nutritious balanced meals. Usually give small portions and gradually the patient resumes normal feeding 6. Hygiene maintained through daily bath and frequent changing of soiled linen 7. Elimination- provide bedpan in acute phase. As patient improves allow ambulation to the toilets  18 July 2024 75 Management 8. Infection prevention to include hand washing, gloving, and disinfection of contaminated articles and linen. 9. Psychological care 10. Health education on the: Disease Preventive measures to include personal hygiene, food hygiene and environmental hygiene Diet Drug compliance 18 July 2024 76 Complications 1. Hypovolaemic shock 2. Toxaemic shock/ toxic mega –read more on this 3. Intestinal hemorrhage 4. Peritonitis 5. Intestinal perforation 6. Anaemia 18 July 2024 77 Prevention and control 1. Adequate treatment of case with appropriate antibiotics 2. Isolation of cases especially in acute stage 3. Screening and treatment of asymptomatic carriers 4. Exclude cases and carriers from handling food especially in the institutions and eating places 18 July 2024 78 Prevention and control 5.Hygienic kitchen practices 6. Personal hygiene practices 7. Environmental hygiene – elimination of flies, proper disposal of human excreta, proper refuse disposal, good sanitation, safe water supply. 8. Notification of the disease locally and internationally 18 July 2024 79 Prevention and control. 9. Disinfection of articles / linen contaminated with stools of infected persons 10. Screening of food handlers 6 monthly 11. Health education of the public on the disease and preventive measures 18 July 2024 80 Questions?? 18 July 2024 81 THANK YOU