Parasitology MBS 600 - 2024 Lecture Notes PDF

1|Page THE COPPERBELT UNIVERSITY SCHOOL OF MEDICINE DEPARTMENT OF BASIC SCIENCES MEDICAL PARASITOLOGY LECTURE NOTES LECTURER: PROFESSOR VICTOR MWANAKASALE “The art of medicine lies not only in knowledge but in the sacrifices made to al...

1|Page THE COPPERBELT UNIVERSITY SCHOOL OF MEDICINE DEPARTMENT OF BASIC SCIENCES MEDICAL PARASITOLOGY LECTURE NOTES LECTURER: PROFESSOR VICTOR MWANAKASALE “The art of medicine lies not only in knowledge but in the sacrifices made to alleviate the suffering of humanity.” – Clinton Simwambi. EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 2|Page Contents 1 SCHISTOSOMIASIS (BILHAZIASIS OR SNAIL FEVER)....................................................................................... 3 2 TRICHOMONIASIS...................................................................................................................................................... 14 3 AMOEBIASIS................................................................................................................................................................ 17 5 ONCHOCERCIASIS..................................................................................................................................................... 27 6 LEISHMANIASIS.......................................................................................................................................................... 33 7 DRACUNCULASIS....................................................................................................................................................... 41 SOIL TRANSMITTED HELMITHIASIS AND ENTEROBIASIS.......................................................................... 45 8 ASCARIS LUMBRICOIDES...................................................................................................................................... 45 9 HOOK WORM INFESTATION................................................................................................................................. 49 10 TRICHURIASIS.......................................................................................................................................................... 52 11 ENTEROBIASIS........................................................................................................................................................ 54 12 TAENIASIS................................................................................................................................................................. 56 13 CYSTICERCOSIS...................................................................................................................................................... 62 14 STROGYLOIDIASIS................................................................................................................................................. 64 15 GIARDIASIS............................................................................................................................................................... 70 17 CYSTOISOSPORIASIS.................................................................................................................................. 79 HEPATOBILIARY, PULMONARY AND INTESTINAL FLUKES (TREMATODES)......................................... 86 19 INTESTINAL FLUKES............................................................................................................................................. 86 HEPATOBILIARY & PULMONARY FLUKES......................................................................................................... 88 20 BILIARY:……………................................................................................................................................................. 88 21 HEPATIC: FASCIOLIASIS....................................................................................................................................... 90 22 PULMONARY FLUKE: (PARAGONIMIASIS)....................................................................................................... 93 23 TOXOPLASMOSIS................................................................................................................................................... 96 Thank you...................................................................................................................................................................... 106 “The greatest sacrifice is when you sacrifice your own happiness for the sake of someone else.” – Julandie Scholtz EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 3|Page 1 SCHISTOSOMIASIS (BILHAZIASIS OR SNAIL FEVER) It is a neglected tropical disease. Causative agent: Flat Worm (Phylum - Platyhelminthes) Class: Trematodes - Leaf Like (fluke) Organism. Since found in blood - Blood flukes, Group/Genus: Schistosoma Species: 3 main species  Schistosoma Haematobium  Schistosoma Mansoni  Schistosoma Japonicum. Less common & less wide spread species (GIMM)  S. Mekongi  S. Intercalatum  S. Guineensis (Newly diagnosed)  S. Malayensis Brief History: First described in 1851 by a young German doctor - Theodore Bilharz who was working in Cairo - Egypt, and found thread like worms in a Human Liver Autopsy. Male adult worms measured: 1cm, female adult worms measuring: 1.2cm - 1.6cm. These worms are constantly together throughout their lives. MODE OF TRANSMISSION:  Infection is acquired by direct skin contact of man with fresh water which has free swimming larva stage of the parasite known as Cercaria (Infective stage)  It penetrates the skin of human and other reservoir hosts.  When it penetrates the skin, it loses the bifurcated tail and becomes a schistosomulum, which now enters the capillaries and lymphatics and passes through the heart to the lungs.  After several days it migrates from the lungs to the portal venous system in the liver. They pair up (male and female) & maturation and mating occurs from there.  After pairing, they will migrate to different veins depending on the species. S. Mansoni pairs migrates to the Superior Mesenteric Veins S. Japonicum to the Inferior Mesenteric Veins S. Haematobium to the Vesical Plexus and the Veins draining the Ureters  Eggs production occurs 4-6 weeks EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 4|Page  Pairs can live 3-4 years in the veins but can live up to 20 years.  The eggs pass from the veins into the adjacent tissues and find themselves in the: Intestinal mucosa then intestinal lumen and are shade in faeces for (S. Mansoni and S. Japonicum), Ureters and bladder mucosa then the eggs are passed out in urine (S. Haematobium) The life cycle is completed when the eggs hatch in fresh water to produce a Motile ciliated structure called Miracidium which goes to invade the fresh water snails. FRESH WATER SNAILS:  S. Haematobium – Bulinus (genus)  S. Mansoni - Biomphalaria  S. Jepanicium - Oncomelania specie (This snail is Amphibian meaning found on both Land and fresh water).  In the snails the miracidium undergoes development to produce Cercaria which are released in water to infect human.  S. Mansoni and S. haematobium mainly infects humans.  S. japonicum mainly infects animals and humans who happens to be the host (water buffaloes, dogs and pigs) SPECIES HOST S. Hematobium Man, rarely Monkey (not zoonotic) S. Mansoni Man, sometimes Baboons, animals (not zoonotic) S. Japonicum Animals - Dogs, Cats, Pigs, Rodents, water buffalos, humans (Zoonotic) S. Intercalatum Man only S. Mekongi Dogs mainly then humans (Zoonotic) S. Guineensis Man only S. Malayensis Rodents mainly, then humans (Zoonotic) EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 5|Page Snell intermediate hosts for less common species  S. Guineensis = Bulinus  S. Intercalatum = Bulinus  S. Malayensis = Robert Siella  S. Mekongi = Neotricular LIFECYCLE OF SCHISTOSOMA SPECIES EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 6|Page EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 7|Page EPIDEMIOLOGY Has the second highest prevalence in the tropical countries after malaria and a leading cause of severe morbidity in the large part of Africa.  600 million people at risk, 200 million infected, 20 million people severely sick worldwide.  85% of schistosomiasis is found in Africa.  Urinary schistosomiasis is found in 53 countries in Africa, Middle East.  Intestinal schistosomiasis is found in 55 countries including Africa, Asia and South America. GEOGRAPHICAL DISTRIBUTION SPECIES TYPE LOCATION S. Hematobium Urinary Africa, Middle east Schistosomiasis S. Mansoni Intestinal Africa, Middle east, South America S. Intercalatum Intestinal West and Central Africa S. Mekongi Intestinal Along the Mekong basin of Cambodia S. Japonicum Intestinal South East Asia, far east S. Guineensis Intestinal West Africa S. Malayensis Intestinal South east Africa POPULATION AT RISK  School aged children in their second decade of life 10-20 years.  Certain occupations such as fisherman, Irrigation workers (sugarcane plantations), women and girls. CLINICAL PRESENTATION GENERAL  Pathology depends on the stage/intensity of infection. Chronic symptoms are related to total worm- load meaning the number of worms.  Light infections (few) are usually asymptomatic in schistosomiasis there is negative binomial distribution in the community.  Immunity is developed and directed against the schistosomulum  In an endemic area individuals acquire immunity and many adults will show few or less signs and symptoms.  Adult worms evade the immune system.  Immunological reactions directed at the eggs stage of the parasite is responsible for most of the pathology in schistosomiasis and hence schistosomiasis is termed an immuno-pathological disease. EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 8|Page SPECIFIC SWIMMERS ITCH aka (KABURE ITCH) or Cercaria dermatitis and occurs where the parasite invaded the skin (S.M, S.J, S.H) (Slight Erythema and pruritic papules in all the 3 species). It is more frequent and violent if is due to animal schistosomiasis (BIRD). However, it is cleared by the human immune system ACUTE SCHISTOSOMIASIS/ KATAYAMA SYNDROME (FEVER) is a form of acute schistosomiasis and occurs with S. Mansoni and S. Japonicum as a result of immunological reactions to substances released by the eggs, occurs 4-8 weeks after infection (when female worms start producing eggs). FEATURES: More frequently with S.M & S.J, less frequently with S.H  Fever  General discomfort  Abdominal pains  Diarrhoea  Vomiting  Myalgia  Arthralgia  Cough  Urticaria  Flu-like illness  Wheezing  Lymphadenopathy  Wheezing  Hepatosplenomegaly EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 9|Page ECTOPIC LOCALIZATION (Localization of either eggs or adult worms in an unusual locations e.g. spinal cord and the brain). a) CNS Spinal cord - Transverse myelitis (common with S.H & S.M)  Patient presents with Spatial paraparesis due to spinal cord compression by granuloma or adult worms. Brain – Picture similar to cerebral vascular accident (Hemiplegia, Epilepsy) especially with S.J b) SKIN - Papular dermatitis CHRONIC INFECTION  50% of the eggs are excreted in stool or urine and most of the remaining 50% die locally or are transported back to the liver others get trapped in the small vessels.  The eggs and the digestive juices they produce bring about local inflammation.  Lesions are explained as a result of local inflammation (granuloma formation, the granuloma maybe 1000times than the size of the egg) and most of the cells are eosinophils. Granuloma heals by fibrosis and causes loss of tissue elasticity. a) INTESTINAL SCHISTOSOMIASIS  By S.Mansoni and S.Japonicum PRESENTATION  Diarrhoea - blood + mucus  Pseudopolyps - colon  Fibrosis of the intestines  Hepatosplenomegaly associated with esophageal varices (due to collateral blood circulation) and there is Ascites  There is fibrosis in the liver which is called Periportal fibrosis also known as SYMMERS CLAY PIPESTEM b) URINARY SCHISTOSOMIASIS (RENAL AND URINARY BLADDER) Causative Agent: Schistosoma Haematobium  Eggs can be found in urinary bladder, rectum, prostate, vagina, cervix, ovaries and uterus 1) There is haematuria as result of bleeding from urinary bladder (terminal haematuria). Bleeding is due to shedding of eggs. EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 10 | P a g e Classification of haematuria  Total haematuria  Initial haematuria  Terminal haematuria  Symptoms are seen in school aged children.  Before treatment the lesions are polyps, ulceration, genitals, white like growth or pannus erosions 2) Ureteric Stricture in the distal 1/3 of ureter caused healing of Granuloma by fibrosis. Presents with hydroureter or hydronephrosis, vesicoureteral refluxes) all these are reversible condition. 3) Linear calcification of the retained dead eggs 4) Transformation into squamous cell carcinoma 5) Reduction in bladder capacity GENITAL Female genital schistosomiasis infection which may result into  Vaginal Discharge, Dyspareunia, Dysuria with complications such as infertility and ectopic pregnancy. Male genital schistosomiasis infection - Haemospermia RENAL  Only cause by S. Mansoni can cause glomerulonephritis due to immune complexes deposition. CARDIAC AND PULMONARY Lesions caused by S. Mansoni and S.Japonica as a result of collateral circulations due to Portal Hypertension which cause Cor-pulmonale because the eggs are washed back to the lungs causing fibrosis and pulmonary hypertension. S. intercalatum affects mostly the rectum hence called Rectal Schistosomiasis. DIAGNOSIS  Clinical: Series of question from a Questionnaire for symptoms and signs, e.g., if they passed blood in urine, check urine for blood and color.  Light microscopy of stool (for S. mansoni, S mekongi, S.japonicum and S. intercalatum) and urine (for S. haematobium). EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA)  11 | P a g e Urine Examination – S. haematobium  Use urine microscope and/or urine filtration methods. Report as Egg/10ml Stool Examination – Other Species  Kato-Katz methods (Formol-Ether Concentration). Report as Eggs/gram Supply 2-3 samples for diagnosis to be made. The eggs under microscopy have the following spines  S. haematobium - Terminal spine  S. mansoni - Lateral spine  S. japonicum – Rudimentary spine  S. intercalatum - Terminal spine (Acid Alcohol Fast - Positive on ZN – Eggs will stain Pink) Serology  Ab detection or Ag detection. Ag detection shows whether a person has the infection or not Ab detection is not very helpful, as it only shows that a person had an infection before. Others: Reagent Strip (Multistix) - For Micro-hematuria Imaging  US – hydronephrosis, hydroureter and staging of fibrosis.  Plain Abd X-Ray/ KUB - linear calcification of the bladder  IVU/ IVB  CT – Scan – Shows the degree of fibrosis of the Liver Biopsy = rectal biopsy/ rectal snip - detects more S.H than S.M Examine for eggs (S. haematobium and S. mansoni) Eosinophilia Endoscopy  Esophagoscopy - (check for varices)  Cystoscopy - (looking for sand patch appearance due to S. haematobium) EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 12 | P a g e TREATMENT  Drug of choice is Praziquantel 40mg/kg single dose (if a scale is available)  Without a scale use dose pole which gives about 30-60 mg/kg Praziquantel.  Tartar Emetic aka Antimony tartrate was used to treat Leishmaniasis and Dr. J.B Christopherson a British Doctor who was working in Sudan observed that, when he gave the drug to treat Leishmaniasis in patients who also had Schistosomiasis found that the drug could make eggs for S. haematobium to disappear from stool.  Niridazole – S. haematobium (ambilhar)  Metrifonate  Oxaminiquine (S. mansoni)  The new drugs on standby in case of resistance to Praziquantel are Oltipraz and Mirazid. CONTROL 1. Preventive chemotherapy using praziquantel (mass treatment or target e.g school or selective treatment). 2. WASH – Water Sanitation And Hygiene  Health education  Safe Water Supply  Improvement sanitation 3. Snail Control (Copper Sulphate), Microsamide, Metaladehyde. 4. Use mechanized farming EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 13 | P a g e EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 14 | P a g e 2 TRICHOMONIASIS Causative agent: Trichomonas vaginalis a protozoan.  T. vaginalis is a protozoa and exist as flagellates.  Similar morphology to trichomonas vaginalis are;  T. Tinax (found in the mouth) it is nonpathogenic (commensal)  T. Pentatrachomonas hominis (found in the large intestines). History Was first described in 1836 by Alfred don in abnormal vaginal discharge from a woman that had vaginosis. MODE OF TRANSMISSION 1. Main mode of transmission is through sexual intercourse. a) Prevalent in heterosexuals, b) Prevalent in high sexual activity age group, c) Also high in patients that have other STI’s. d) Less common in low sexual activity age group i.e., before puberty and menopause in homosexual. e) Less common in homosexuals as well. 2. Mechanical transmission through – a) Sexual partners via the fingers and b) Via vibrators. 3. Non sexual contact transmission occurs because the protozoa are able to survive for a long time if kept in moist places or environment e.g. contaminated toilet seats, shared sponges or towels and communal bathing. EPIDEMIOLOGY T.V is probably the most prevalent non-viral STI in the world, where we have 170 million people with new cases every year. T.V promotes transmission of HIV, may lead to preterm delivery, low birthweight Common in low social economic status, and low levels of education and douching CLINICAL PRESENTATION WOMEN 10-50% are asymptomatic, one third develops symptoms within 6 months EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 15 | P a g e Specific Symptoms  Vaginal discharge (yellowish discharge, sometimes the discharge may be purulent), vulval itchiness, strawberry cervix - macular erythematous lesion called COLPITIS MACULARIS which is seen via colposcopy.  Non-specific symptoms  Dysuria  Dyspareunia  Vulval-vaginal sores. History of multiple infections (STIs) Incubation period is 5-28 days after sexual contact. MEN TV is isolated in 14% - 60% in men whose partners have TV  Most cases are asymptomatic,  Responsible for 5-15% of non-gonococcal urethritis (Urethral Discharge is scanty)  Incubation period is 3-8 days LABORATORY DIAGNOSIS 1. Wet mount a) Collected specimen (High Vaginal Swab, Urethral discharge (urethral scrap) or Prostate fluid, alternatively centrifuge the urine and examine) to be examined under 10 minutes of collection. b) You will see diagnostic jerky movement or falling leaf or like a ghost (visible movements but parasite can’t be seen). c) Examination can be done with no staining by wet mount, black-field/light microscopy, dark- field microscopy) d) 50 -75% of infected women will be picked by wet mount e) 1- 20% of infected men will be picked by wet mount 2. Fluorescent microscopy using Acridine Orange dye. 3. Pap smear (not for diagnosis) you may see TV incidentally. (Sensitivity is very low) 4. Culture method is the most sensitive for making diagnosis (Gold standard). a) Up to 85% Sensitivity and 100% Specificity. b) Culture is done using a medium called Diamond TYM medium. Incubation is done and results are ready by 48 hours. (Cumbersome method) EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 16 | P a g e c) In-pouch TV system method (More convenient) can also be used (same sensitivity with diamond TV). The inoculation is examined immediately or incubated to be done under 1 hour of sample collection. Can do direct examination under microscope if TV not seen then you can incubate for 48hr 5. Serology-Ag detection. ELISA results ready within 10minutes 6. PCR can also be done TREATMENT 5-Nitromidazole compounds are used  Metronidazole/ Flagyl (2g Single dose or 500mg BD for 7days)  Tinidazole 2g Single dose EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 17 | P a g e 3 AMOEBIASIS  Causative agent: Entamoeba histolytica  It has a cosmopolitan distribution (found worldwide).  Transmission depends on the levels of personal hygiene and sanitation.  Moves by pseudopodia   First described in 1875   Trophozoites of Entamoeba histolytica resemble Entamoeba chattoni which infects monkeys and rarely human.  Cysts of Entamoeba histolytica resemble a non-pathogenic parasite called Entamoeba dispar.  MODE OF TRANSMISSION  Faecal-oral route by ingestion of the cystic stage of the parasite via direct contact, person-to-person or contaminated water and food with the cyst.  Contamination of food can occur via cockroaches and flies.  Sexual intercourse (Oral-anal)  LIFE CYCLE  Infection is caused by the ingestion of the cystic stage of the parasite.  The cyst undergoes excystation in the small Intestines to develop motile trophozoites.  Trophozoites migrates to the colon and invade the Colonic Mucosa, and multiply by (binary fission) asexual reproduction. After several multiplication the trophozoites undergo encystation to form cysts in the colon and thereafter the cysts are excreted in stool.   In stool there will be two stages:  Trophozoite stage: Dies fast outside the body and are not responsible for transmission.  Cyst stage: found in the lumen of the colon and not in the tissues. EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 18 | P a g e EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 19 | P a g e CLINICAL PRESENTATION There are two forms which are Intestinal and Hepatic amoebiasis. Intestinal amoebiasis has 4 forms. The patient may be asymptomatic. Pt may present with amoebic colitis. May present with fulminate colitis. May present with amoeboma. ASYMPTOMATIC AMOEBIASIS  Trophozoites in the large intestines may remain for several years without causing any damage in about 90% who are carriers.  Detection is after examination of the stool and finding presence of trophozoites. AMOEBIC COLITIS  Incubation period varies and the Entamoeba histolytica penetrates and invades the intestinal mucosa of colon causing ulceration with eroded undermined edges of the ulcers and the ulcer look like a button hole. Clinical Features include;  Abdominal pains,  Bloody Diarrhoea or Dysentery.  Moderate fever or no fever  Patient’s general condition is good  Patient may present with tenesmus.  Perianal ulcers. FULMINANT COLITIS (SEVERE FORM)  Fever  Severely ill  Paralytic ileus  Intestinal bleeding  Perforation of the colon with seepage of intestinal content This Fulminant form maybe part of progression of the disease from amoebic colitis to severe form or when a patient is wrongly diagnosed for Ulcerative colitis or Crohn’s disease and put the patient on steroids. Steroids given worsen the condition from Amoebic Colitis to Fulminant Colitis. EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 20 | P a g e AMOEBOMA  1% may develop this, there is inflammatory thickening of the intestinal wall, such that you can palpate the swelling on Abdominal Examination.  Diagnosis is made by biopsy and you will find trophozoites. DIAGNOSIS Laboratory examination  Stool examinations: Fresh stool is examined within 1hour in form of a Wet Mount looking for the motile trophozoites which look like macrophages and the difference is that these trophozoites will have ingested RBCs.  Rectal ulcer swab, both resemble macrophages, motile trophozoites will have RBCs inside.  Formed stool examination: Cysts in the stool. Diagnostic feature is based on number of nuclei (usually 4) and the size of cyst.  Serology: Antigen detection is the Most Sensitive and Specific.  PCR. TREATMENT  No point of treating asymptomatic cases because 90-95% of these are due to Entamoeba Dispar which is non-pathogenic.  Treat food handlers with drugs called Contact Amoebicides which destroy the Cyst Stage (in the distal end of the intestines) which include;  Diloxanide furoate  Iodoquinol  Paromomycin AMOEBIC COLITIS (SYMPTOMATIC)  5-Nitroimidazoles e.g., Metronidazole or Tinidazole clear trophozoites.  In addition, give contact amoebicides to clear the cyst stage.  5-Nitroimidazoles act on the proximal part of the colon while contact amoebicides act on the distal part of the colon. In dysentery give both. EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 21 | P a g e Avoids alcohol intake when someone is on metronidazole. HEPATIC AMOEBIASIS  Parasite trophozoites are transported to the venous blood from the intestines to the Liver, and abscesses form in the liver, pus is made of hepatocytes. The abscess is due to cytolysis of liver tissue. The abscess is not a true abscess because it is made up of dead liver cells. FEATURES:  Fever  Abdominal pain in the Liver region  Referred to the right shoulder  Hepatomegaly  Raised diaphragm  Reactive pleural effusion  Lung infestation (actual lung tissue affected)  Fistula formation between the abscess and skin.  Jaundice DIAGNOSIS:  Clinical presentation  FBC – Leukocytosis  U/S  Antigen Detection is the Most Sensitive  PCR also has high sensitivity and specificity  Aspirate the abscess (colour of pus is called Anchovy sauce – Brownish red) and it is not foul smelling and trophozoites are not found in the pus but at the edge of the abscess.  Trophozoites or cysts in intestines or stool-less than 20%. TREATMENT  Metronidazole plus contact amoebicides  Emetine/Dehydroemetine if patient is resistant to 5-nitroimidazole.  Surgery can be done if the abscess is too big or there are complications or failed medical management. EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 22 | P a g e 4 ECHINOCOCCOSIS (HYDITIDOSIS/ HYDATID DISEASE)  This is a Zoonotic disease occurring as Cystic or Alveolar Hydatidosis.  Causative agent: Tape worm (Flat worm, Phylum – Platyhelminth, Class -Cestode)  Species:  Echinococcus granulosus - (Dog/ Small Tapeworm) causing Cystic Hydatidosis  Echinococcus multilocularis - (Fox Tapeworm) causing Alveolar Hydatidosis CYSTIC HYDATIDOSIS  Definitive hosts are Dogs and other Canines.  Intermediate hosts: Sheep, Goats, Cattle and Pigs.  Accidental Intermediate host: Man MODE OF TRANSMISSION 1. Fecal Oral Route by ingestion of eggs/ova of the parasites from infected dog feces in contaminated water or food. 2. Direct Ingestion of eggs from an infected Dog/Canine that are passed to man e.g., onto the hands of people like dog lovers which are then swallowed. LIFE CYCLE  Intermediate hosts and Man get the infection by swallowing the eggs/ova of the Tapeworm from the dog feces.  Eggs of parasites enters the intestine and hatch into larva.  The larvae called the Onchosphere – Immature larva penetrate the intestinal wall and gets carried via venous blood to the Portal-Venous System (liver).  Larvae matures into a mature stage of the larva called Hydatid cyst which has daughter cysts inside it.  The life cycle is completed when the dog eats the offal of food animals such as Sheep, Goats, Cattle and Pigs that contains the hydatid cysts.  The Daughter cysts ingested by the dog develop into adult worms which starts producing eggs or larva which are excreted in feces. EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 23 | P a g e 24 | P a g e EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 25 | P a g e EPIDEMIOLOGY  The distribution is worldwide but commonest in Kenya and Eastern Europe. CLINICAL PRESENTATION  Infection is usually acquired during childhood and the cysts grow slowly over many years in different organs.  Most cases the condition is asymptomatic.  Symptoms arise due to mechanical consequences (pressure on the organs)  LIVER: Hepatic cysts may lead to massive hepatomegaly, associated obstructive jaundice with or without cholangitis. CNS: Symptoms of space occupying lesions; Epilepsy, Eosinophilic meningitis. BONES: Bone pain, pathological fractures. LUNGS: Usually the patient is asymptomatic, but may develop a cough. KIDNEY: Unilateral destructions of the kidney ALLERGIC REACTIONS: The cyst may rupture spontaneously, due to trauma or surgery. Patient may develop urticaria, bronchospasms, and anaphylactic shock if the cyst ruptures. EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 26 | P a g e DIAGNOSIS  Radiological imaging such as;  Abdominal X-ray, which shows crescent calcification of the cysts  CXR  CT Scan  U/S  During surgery: e.g., during Laparotomy you need to take Biopsy which might reveal Hydatid cysts.  Serology by Antibody detection to detect the Specific IgG e.g., by ELISA, Indirect Hemagglutination Test. TREATMENT  Waiting/Observation for many of the cyst will remain stable for many years, some calcify others disappear/involute.  Chemotherapy. Give Praziquantel (PZQ) or Albedazole (800 mg OD for 8 months) or both (better option)  Large cysts may require surgery (cyst greater 10cm). During surgery give pre-operative treatment with drugs such as albedazole or prizaquental.  Percutaneous treatment (PAIR) - Puncture Aspiration Injection Re-aspiration. With imaging guidance Inject with a hypertonic solution such as 95% ethanol, then re-aspirate. ALVEOLAR HYDATIDOSIS  Cause by Echinococcus multilocularis (Fox tapeworm) MODE OF TRANSMISSION  Fecal-Oral transmission by ingesting eggs or ova in the infected faeces of fox.  Humans get accidentally by eating contaminated wild fruits such as berries or drinking water.  Found in the northern hemisphere (cold climates) e.g. Siberia.  Life cycle, Clinical presentation and Treatment same as Cystic Hydatidosis. EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 27 | P a g e 5 ONCHOCERCIASIS  It is a NTD also called River Blindness.  Not zoonotic  Causative agent: Tissue filarial worm of the species Onchocerca volvulus. MODE OF TRANSMISSION  Only by the Bite of infected female Blackfly of the genus Simulium specie LIFE CYCLE: Refer to filarial life cycle  The infective stage is the L3 (Filariform larva) - Microfilaria  L3 enters the body from the bite wound and it undergoes 2 molts from L3 to L4 then produce L5 (adult worms) which are found in the subcutaneous nodules and in the lymph space.  Subcutaneous nodules are also called Onchocercomata and are usually 2 cm in diameter and are palpable.  The adult worms measure about 2 - 4cm and can live in the human body up to 15years.  Pre-patent period is 12-15 months EPIDEMIOLOGY:  Onchocerciasis is a chronic parasitic infections and the two major features are ocular and dermatological pathology.  Commonest feature is pruritus or itchiness  Most serious presentation is ocular blindness.  For the ocular pathology the final result is blindness and for dermatological its intense itching (pruritus).  Due to its effects it leads to socioeconomic depression.  Endemic in 37 countries and these are West, East and Central Africa, Arabian Peninsula, South and Central America. EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 28 | P a g e  126 million people at risk of the infection and 18 million estimated to be infected and most i.e., 99% are in Africa. Zambia is spared (had a single case though).  It’s one of the 4 major causes of blindness globally. (Cataracts, Trachoma, Glaucoma, Onchocerciasis)  270,000 completely become blind and 500,000 with severely impaired vision.  Onchocerciasis’ cumulative infection (grows over time, builds up with reinfection)  Severity depends on the  Length of exposure to the bite and,  Density of microfilaria in the skin.  In heavily infected communities, prevalence is 70% and only half of these will have symptoms.  15% will have serious skin manifestation and 5% will have blindness.  Geographical variation of the disease:  Clinical pattern of features depends on the geographical variations e.g. the subcutaneous nodules in:  Africa, are found around the pelvic girdle in adults, and found on the upper side of the body e.g. Head in children  Central America, they are found on the head in all age groups.  South America, lower half of the body.  Variations are due to different parasite strains and vector parasite relationship.  In Africa and the Arabian Peninsula the vector is the = Simulium Damnosum species complex.  East Africa = Simulium Neavei species complex  South and Central Americas = Simulium Metallicum.  Simulium Damnosum lay eggs on trailing vegetation in fast flowing river water and rocks because of excess oxygen.  Simulium Neavei lay eggs on Amphibian Crabs. EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 29 | P a g e PATHOLOGY  It is only the female black fly that feeds on the bloody meal. However, both feed on plant juices.  The lesions are as a result of host inflammatory response to dead and dying microfilarial worms, leading to damage of surrounding tissue.  Ideally the living only cause minimal host inflammatory response. EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 30 | P a g e CLINICAL FEATURES  The pattern and frequency of clinical features vary according to; Duration and frequency of exposure, Geographical location and, Individual variation. A. DEMATOLOGICAL FEATURE  The most frequent symptom is itching of the skin, sometimes causing incapacitation associated with excoriation.  Other features like papular eruption which may be anywhere.  Intra-epithelial abscesses  Transient Oedema of the limbs and Lymphadenopathy (inguinal and femoral)  Premature aging of the skin (wrinkled skin, shiny)  Depigmentation of the skin (spot appearance like a Leopard)  Chronic lymphadenopathy with fluid surrounding called the “HANGING GROINS”  Sowda appearance  Subcutaneous nodules B. OCULAR FEATURES  With moderate or severe load of microfilaria there is visual damage affecting all tissues of the eye starts with conjunctivitis with photophobia (may heal without complications).  When the cornea gets affected there is:  Punctate Keratitis - there is acute inflammatory exudate that surrounds the dead and dying microfilaria, resulting in a snow flake opacity resolving without complications and has no sequel.  Sclerosing Keratitis - there is progressive exudative process with fibro-vascular pannus formation which may lead to irreversible visual damage and Blindness. EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 31 | P a g e OTHER OCULAR LESIONS;  Anterior uveitis (leads to blindness)  Iridocyclitis  Chorioretinitis (leads to blindness)  Secondary cataract  Glaucoma  Optic atrophy (leads to blindness)  The degree of visual damage is associated with microfilaria density in the eye.  The prevalence of visual loss increases with age.  At any given age men are 1.5 times more likely to get blindness than women DIAGNOSIS Laboratory 1. Skin strip (get skin biopsy and look for microfilaria) from the iliac crest or calf for Africa. For South America, from the shoulder. Get the skin and put it in NS or distilled water and examine after 30 minutes, 60% of the microfilaria will come out and will be found while 75% will be found under 24 minutes. 2. Light microscopy - look for microfilaria 3. Slit lamp examination and view the microfilaria in the anterior chamber of the eye. 4. Mazzoti test ; Provocative test (you give a patient a small dose of diethylcarbamazine (DEC) and they get pruritic rash) 5. Biopsy 6. Serology: (Current diagnostic method) called an OV 16 antibody test. EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 32 | P a g e TREATMENT SURAMIN IV:  First drug used for onchocerciasis and the only drug which is true macrofilaricide  Side effects: Exfoliative dermatitis, anaphylactic shock, nephropathy, jaundice, diarrhea and mazzoti reaction may result. DIETHYL CARBAMAZINE (DEC)  It has an effective microfilaricidal effect  It has severe side effects such as blindness and death, thus not used. IVERMECTIN  It is a drug of choice and is given orally at intervals of 3-24 months.  Two-third of patients relapse 6 months after being given the drug.  Invermectin causes suppression of microfilaria longer than DEC  Ivermectin treatment is suppressive not curative.  Other side benefits of Invermectin include clearance of Lymphatic Filariasis (Wucheleria bancrofti), Ascariasis, Strongyloidiasis and Scabies.  Make sure you rule out Loa Loa before starting Ivermectin treatment, because the patient will die from encephalitis.  Side effects include fever, skin rash, lymphadenopathy and postural hypertension. PREVENTION AND CONTROL  Protective chemotherapy for treating the affected community regardless of their status by giving the dose of Ivermectin once every year.  Vector control; Spraying where the eggs and larva are emerging from.  Nodulectomy EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 33 | P a g e 6 LEISHMANIASIS  It is a Neglected Tropical Disease.  Invasive parasite  Causative agent is a tissue flagellate belonging to genus Leishmania Sub-genus; (i) Viannia (ii) Leishmania The sub-genus are based on the site of development of the parasites in the gut of the vector which is called Sand Fly.  Viannia develops in the hindgut there after goes to midgut then migrates foregut and this type of development is called the peripylaria.  Leishmania develops in the midgut, there after goes to foregut, and this type of development is called the suprapylaria. Three (3) forms of the disease: 1 Visceral leishmaniasis (Kala azar) caused by; L. L. donovani, L.L. chagasi, 2 Cutaneous leishmaniasis which is in two forms  Old world - by L. L. Major, L. L. Tropica  New world - L. L. Mexicana, L. L. Amazonensis 3 Mucosal also called mucocutaneous or espundia leishmaniasis caused by L. L. (viannia) /brazilienisis MODE OF TRANSMISSION Mainly is by the bite of an infected blood sucking female sand fly (vector)  There are two species of the sand fly Lutzomyia (in America) and phlebotomus (the rest of the world)  The vector is a weak sand fly and resides in vegetation in forested areas, rodent burrows, in arid region (dry land) and also debris around residential areas where you have peridomestic transmission. Others less common methods;  Congenital  Blood transfusion  Person to person contact  Laboratory accidents EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 34 | P a g e LIFE CYCLE  Female sand fly becomes infected when it consumes blood containing amastigote infected macrophages from infected person and they don’t have flagella.  At optimal temperature, the amastigote gets transformed into promastigotes in the gut of the sand fly and thereafter it undergoes multiplications and transform into an infective stage called metacyclic promastigotes in humans.  When they mature, they migrate to the mouth parts of the fly (proboscis) and interfere with the ability of the vector to suck blood then coughs to introduce it into a person.  Only a small amount of promastigotes gets injected into the skin of human beings.  In the macrophages, the parasites lies in phagolysosomes and get transformed into the Amastigotes.  In the phagolysosomes, the amastigotes multiply and rupture and infect other macrophages. EPIDEMIOLOGY  Leishmaniasis is found in all the continents apart from Australia and the Antarctica  Reported in 21 countries in the new world and 62 countries in the old world  350 million people are at risk of cutaneous  Cutaneous affects 1.0-1.5 million/year and visceral affects 150 000/year.  Epidemiology depends on the species of the parasites and geographical locations.  In majority of areas it is a zoonosis and the reservoir hosts are the rodents and canines (dogs).  In some cases it is not a zoonosis e.g., L.L. donovani (humans are the only hosts (in India) (not zoonotic) SYNDROME LOCATION Visceral Asia, East Africa (Kenya, Ethiopia, South Sudan and Somalia), East leishmaniasis Mediterranean, South and Central America. Cutaneous Asia, East Africa (old world ) leishmaniasis New world Central and South America Cutaneous Leishmaniasis and Mucosal leishmaniasis EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 35 | P a g e EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 36 | P a g e CLINICAL MANIFESTATION  Leishmaniasis is a special disease  Wide range of clinical presentation  Clinical manifestation depends on the complex interactions between the virulence characteristic of the Leishmania species that is involved and genetically determined cell mediated immunity. A. Cutaneous leishmaniasis: 1. Simple cutaneous leishmaniasis Lesions develops where the promastigotes are injected in the skin. They can be single or multiple. Incubation period is 2 weeks to several months  Lesions starts as papules increases in size and then ulcerates  Pizza like appearance ulcer which can either be  Wet lesions (exudate)  Dry lesions (smaller) 2. Diffuse cutaneous leishmaniasis Plaque like or nodular lesions which may develop on the face and any other exposed areas on the body and they don’t ulcerates. 3. Leishmaniasis Recidiva Chronic localized lesion and they persist for year and classically there is healing from the center and they are typically seen on the face and other exposed areas. B. Mucosal Leishmaniasis  Causes Espundia (occurs in Americas) and there is healing of the cutaneous leishmaniasis followed by development of the obstructive mucosal lesions and may occur after several months or years.  The nose is the organ that is frequently affected and patients develops nasal stuffiness, discharge and discomfort.  Overtime the nasal septum gets destroyed and results in the nasal collapse and development of “Tapir nose”  Lips, oropharynx and larynx may also be affected.  If it persist there is substantial disfigurement.  Cause of death is chronic aspiration pneumonia. EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 37 | P a g e C. Visceral Leishmaniasis  Aka Kala-Azar or Dum-Dum fever.  Incubation periods: 10days - 34 months (several days to months) in immunocompetent individuals  May occur as an opportunistic infection in immunocompromised patients. Clinical features a. Subacute fever b. Body Weakness c. Fatigue d. Weight loss e. Massive splenomegaly (Kala-Azar - Differential Diagnosis) f. Hepatomegaly g. Acute fever resembling Malaria (illness may be continuous or intermittent - Two spike of fever in a day) h. Hyperpigmentation of the Skin called black fever or kala azar. Lab findings a. Anemia b. Leukopenia c. Thrombocytopenia d. Hypergammaglobulinemia If the condition is not treated death may result. Even after treatment death occurs in 10%. Visceral Leishmaniasis with HIV infection  This is considered an opportunistic infection.  Patient present with fever, splenomegaly and hepatomegaly  Prognosis is poor without HAART(improved with HAART) Visceral-tropic leishmaniasis,  observed first in soldiers who returned from the gulf war (fever, malaise, fatigue and massive splenomegaly) EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 38 | P a g e Post Kala-Azar Dermal Leishmaniasis  It develops after the patient has undergone chemotherapy for visceral leishmaniasis.  Occurs in Africa and India.  It is a skin condition characterized by nodular, macular, or papular lesions on the face, trunk and extremities. Presents like leprosy. Individuals with the condition serve as reservoirs of the infection. DIAGNOSIS 1. Clinical syndrome plus history of exposure 2. Parasitological examinations looking for the Amastigotes in the clinical specimen (biopsy, aspirates, touch, bowel perforations) then stain with any Romanoski stains such as Giemsa stain. Specimens: i. Skin biopsy - taken from the edge of the ulcer. ii. Splenic aspiration with a fine gauge needle for visceral leishmaniasis (risk hemorrhage) iii. Bone marrow aspiration (for visceral leishmaniasis) to avoid haemorrhage; collect from the iliac crest - sensitivity is 60-80%. iv. Liver biopsy (for visceral leishmaniasis) v. Lymph node aspirate or biopsy (for visceral leishmaniasis) vi. Culture can also be done from the biopsy, or bone marrow aspirates. Media: NNM (Novy Nicole Mcneel), Schneider insect medium. vii. PCR viii. Serology (Method of choice, looking for specific Anti-leishmania antibodies): IFAT, ELISA, Direct Agglutination Test (DAT can also detect antigens). Antibodies are raised in immunocompetent and absent in HIV. ix. Leishmanin skin test (Montenegro test) look for a well: Inject portion of parasite antigen into the skin to detect delayed hypersensitivity response (Type IV) to the antigen. The test is negative if patient has progressive visceral leishmaniasis. EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 39 | P a g e TREATMENT Optimal treatment depends on the infecting Leishmania species and the clinical syndrome. Drugs 1. Pentavalent antimony containing drugs  Sodium Stibogluconate (pentostam)  Meglumine antimonite (glucatimine). Side effects and increased treatment failure IV/IM 2. Amphotericin B Deoxycholate (its effective but toxic) was switched to 3. Liposome-encapsulated and lipid associated Amphotericin B (AmBisome). Drug of choice targets the Amastigotes in the macrophages. Used for all clinical syndromes. 4. Pentamidine (Toxic and causes postural hypotension, bone marrow suppression, nausea, vomiting and reversible azotemia). 5. Interferon Gamma (recombinant interferon-gamma) PREVENTION AND CONTROL 1. Diagnosis and treatment, 2. Vector control-residual spraying-DDT and ITN, 3. Personal protective (permethine impregnated clothing), 4. Killing stray dogs, 5. Destruction of where rodents reside. EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 40 | P a g e EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 41 | P a g e 7 DRACUNCULASIS It is a Neglected Tropical Disease. Also known as a Guinea Worm or Medina Infection. Causative agent: by a nematode Dracunculus medinensis (it is tissue filarial worm). MODE OF TRANSMISSION  Infection is acquired by drinking water contaminated with a parasite crustaceans belonging to genus cyclops, which is infected with larva (L3- Filariform Larva), the cyclops belonging to a class called copepod. L3 is the infectious stage found in fresh water. LIFE CYCLE  Cyclops swallowed through drinking contaminated water, reaches the stomach and gets digested, Cyclops release the L3 which penetrates either the stomach or intestines through to the peritoneum  In the peritoneum, the larva undergoes two maturation from L3 to L4, finally L5 (adult form).   3 months after infection, there is copulation and the male worm dies while the female remains over the next 12months and grow to a full size of 60-100cm and 0.5 - 5mm diameter (Longest lifecycle of the worms).  Infected person may tolerate this for about a year.  After 1 year the female migrates to lie next to the skin surface especially of the legs and there is blister formation which occurs as a result of toxic secretion from the mouth of the parasite. The blisters bursts when it comes in contact with water and forms an ulcer.  Each time an infected person goes to the river to relieve the pain, a portion of the worm starts to come out and the L1 (Rhabditiform larva) are released through the mouth. L1 is swallowed by the cyclops in which it undergoes into 2 molting from the L1 to L2 then L3 (the infective stage) to complete the cycle.  Parasites are also found in monkeys, baboons and dogs but it is not a zoonosis. EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 42 | P a g e 43 | P a g e EPIDEMIOLOGY  Only 6 countries (as of 2020) were endemic in the world, Chad, Ethiopia, South Sudan, Angola, Cameroon, and Mali.  Only 27 cases reported.  It is targeted by WHO for eradication  CLINICAL FEATURES  Painful blister found on the lower leg and feet and pain is alleviating by Deeping in cold water.  Ulcer   Worm may be seen  Abscess may be the first sign seen sometimes  Inflammation near the joints which will lead to arthritis  Contractures which will lead to deformities  Bacterial superinfection TREATMENT  Removal of the adult worm by coiling e.g., using a match stick while keeping the wound moist and may take up to 14 days.  If no inflammation, surgical removal with local anesthesia but if there is inflammation, give anti-inflammatory drugs such as Metronidazole, Niridazole, Thiabendazole, Mebendazole, oxamniquine (though controversial).  Treating the bacterial infection if there is one. Give ATT. EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 44 | P a g e Dracunculiasis life cycle EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 45 | P a g e SOIL TRANSMITTED HELMITHIASIS AND ENTEROBIASIS  They are intestinal nematodes (round worms).   Require soil condition for completion of cycle.  They comprise of: 3  Ascaris lumbricoides  Hook worms (Ancylostoma duodenale and Nectar americanus)  Trichuris trichura. 8 ASCARIS LUMBRICOIDES  A large intestinal nematode.  It is a geo-helminthic parasite,  Transmission is favored by conditions that improve survival of eggs in the soils [warm, moist and shady conditions] MODE OF TRANSMISSION Faecal-oral route by ingestion of the eggs of the parasite. 1. Direct contact with soil 2. Poor hygiene 3. Ingesting contaminated water or food 4. Ingesting contaminated green vegetables not thoroughly washed and were fertilized by human excreta (night soil) LIFE CYCLE  Parasites has a cosmopolitan distribution especially in the tropics.  Infected person passes on the fertilized eggs in stool onto the ground and which requires 10-40 days in the soils for them to become mature and infectious.  Therefore direct self-infection is not possible  Man acquire the infection via contamination of food, drink, and dirty water and grounds.  In the intestines the larva hatches from the egg and penetrates through the mucosa in the intestinal wall to reach the portal venous system and from the liver the larvae are taken to the lungs (3-14 days) where they migrate onto the bronchi and the larva gets swallowed the second time and reaches the intestines in the jejunum where it grows into adult worms. Adult worms are found in the lumen of the jejunum, but do not penetrate the walls.  Copulation occurs, eggs laying occurs after 2 months from egg swallowing. EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 46 | P a g e EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 47 | P a g e EPIDEMIOLOGY  Cosmopolitan in distribution and it’s the commonest worm infestation in humans.   The population at highest risk - children 6-10 years.  Eggs are very resistant to the hostile external environment and they can survive for a long time.  The number of eggs is the measure of hygiene standards and degree of sanitation levels.  CLINICAL PRESENTATION  Majority of cases are asymptomatic.   Abdominal discomfort   Serious complications are rare.  Lung passage symptoms include;  Mild to severe cough  Chest/thoracic pains  Fever  Dyspnoea The above clinical features are collectively referred as Loeffler’s syndrome. Sputum examination: Presence of eosinophils, Larva, crystals called Charcot-Leyden crystals.  Obstruction of the hollow organs:  Intestinal obstruction if they are many  Biliary tract obstruction [Jaundice, cholestasis, cholangitis and  Pancreas - Pancreatitis  Appendix - Appendicitis  Vomiting worms  Intestinal surgery (recent) the worms might breach the suturing.  Malnutrition because the worms feeds on nutrients.It does not cause malnutrition but if the child is borderline then it will take the side of malnutrition.    EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 48 | P a g e  LABORATORY DIAGNOSIS  Microscopy - stool examination using Formol-Ether Concentration or Kato-Katz.  FBC/DC - Eosinophilia  Abdominal X-Ray - see adult worms  Chest X-Ray – Migratory infiltrates in the chest  Barium meal - follow through  TREATMENT  Benznidazole compounds   Mebendazole (vemox) 500mg BD 3 days  Flubendazole(fluvermal)  Albendazole (zentel) 400mg single dose  Piperazine  Pyrantel Pamoate (Combatrin) 10mg/kg single dose  Ivermectin 150mg/kg single dose  PREVENTION AND CONTROL  Preventive chemotherapy through deworming programs 2times a year - child health week   WASH  Thoroughly washing and cooking green vegetables  Improved personal hygiene and sanitation  Health education  Avoid using night soil as fertilizer  Washing of green vegetables in a tincture of Iodine or potassium permanganate EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 49 | P a g e 9 HOOK WORM INFESTATION Causative agents: Ancylostoma duodenale and Necator americanus MODE OF TRANSMISSION  Percutaneous penetration (both) with the L3 larva (Filariform larva)  Oral route of L3, only applies to Ancylostoma duodenale LIFE CYCLE  Adult worms are found in the small intestines and measures about 1cm length.  It lives for few months in the body and produces the eggs which are passed to the soil in the stool.  After about a week in the soil the egg hatches into L1, L2 and L3. (The L2 can survive for weeks, months even up to 2 years if the condition are favorable or optimal temperature and humidity (Neutral pH of soil, high temperature, shady conditions).  L3, the infective stage develops in the soil and penetrates the skin of man (bare footed) or swallowed, for Ancylostoma duodenale and has no lung involvement.  Before reaching the large intestines the L3 after penetrating into the skin goes to the heart and then the lungs and enters the small intestines.  Ancylostoma duodenale infestation can be acquired by eating raw or uncooked meat (Paratenic host – host that is not necessary for completion of the parasitic life cycle e.g. pigs, cattle, sheep, rabbits) The L3 reside in the muscles of these animals.  Adult worms burrows in the mucosa of the small intestines  A. duodenale sticks to the mucosa by teeth/hooks while N. americanus is by buccal cutting plates/blades.  A. duodenale sucks about 5-10 times more blood than N. americanus  N. americanus sucks about 30microLiters/day. (260microLiters/day for A. duodenale) Ancylostoma Necator duodenale americanus EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 50 | P a g e EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 51 | P a g e EPIDEMIOLOGY  Ancylostoma duodenale is found in the old world as while as the new world (Asia, Americas).  Necator americanus is mainly found in the new world and also is found in Africa (Americas, Africa, and Asia). CLINICAL PRESENTATION  The worms live for 5-15years.  Ground itch - rash and Itchiness at the site of L3 penetration (wound itch)  Loffler’s syndrome (passage) only with percutaneous mode of transmission  Anaemia ( Microcytic, hypochromic anaemia)  Hypoproteinemia  Oedema  Geophagia  LABORATORY DIAGNOSIS  Fresh stool Examination (within 24 hours otherwise the eggs will degenerate or hatch in to L1) looking for eggs or ova – FEC or Kato-Katz if available  Blood – FBC - Eosinophilia TREATMENT  Benznidazole   Pyrantel Pamoate (Combatrin)  Ivermectin  PREVENTION AND CONTROL  School health programs  Health education  Preventive chemotherapy via child health week  The WASH  Encourage wearing of shoes  Improved sanitation EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 52 | P a g e 10 TRICHURIASIS  Caused by: Trichuris Trichura  It’s also called Whipworm. MODE OF TRANSMISSION  Faecal-oral transmission  By ingesting eggs via the soil  Self-infection is possible via anal oral route Adult worms have a thin tail which it uses to burrow itself in the large intestines. LIFE CYCLE EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 53 | P a g e  Eggs are passed in stool out of the infected person and they are swallowed or first go to the soil then swallowed.  1 week later, adult worm (measuring 3 – 4cm) will form in the intestines and  Egg laying 2 months after, later fertilization occur after copulation. Adult worms are found in the large intestine and burrow themselves in the mucosa. CLINICAL PRESENTATION  Most of the cases are asymptomatic. Symptoms develops only when there is severe infestation and include;  Diarrhoea (dysentery-like)  Malnutrition  Anemia  Chronic Diarrhoea in undernourished children  Rectal prolapsed – Adult worms can be seen  Tenesmus  Impaired cognitive function, in school going children. (primary) DIAGNOSIS 1. Stool examination - Using Formol-ether Concentration or Kato-Katz (Eggs have bipolar plugs)  2. Rectoscopy TREATMENT  Benznidazole compounds  PREVENTION AND CONTROL  Preventive chemotherapy via child health week  The WASH EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 54 | P a g e 11 ENTEROBIASIS  The causative agent is Enterobius vermicularis   The worm is also called the Seat-Worm or Pinworm or and (Oxyurids) MODE OF TRANSMISSION  Faecal oral route (ingestion of eggs) EPIDEMIOLOGY:  Cosmopolitan LIFE CYCLE  After swallowing of the eggs, eggs turn into larvae and then into adults worms which congregate at the ileocecal junction.  After copulation the male worms dies and female worm will survive and grow up to 0.8 – 1.3cm length.  Female worm migrates via the colon to the anal region and at night the adult female worms lay eggs at the Perianal region.  CLINICAL FEATURE  Pruritus Ani  Nightly Perianal itchiness  Vaginal itchiness (rarely in females) DIAGNOSIS  Stool examination – FEC - looking for the eggs under a microscopy  Scotch tape technique especially in the morning  Urine examination – eggs as a result of contamination  Adult worms in the vaginal swab  TREATMENT  Benznidazole compounds  Vanquin PREVENTION AND CONTROL  If one child is found infected, treat all other children in the family and encourage mother to be changing pants for the children frequently.  EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 55 | P a g e EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 56 | P a g e 12 TAENIASIS  It is a NTD (Neglected Tropical Disease)  Causative agents:  Taenia solium (pork tape worm)  Taenia saginata (beef tape worm)  Taenia Asiatica/Taiwanensis – similar to T. saginata but transmitted via eating raw pork.  Cestodes -Tapeworm or plathelminth MODE OF TRANSMISSION  Via oral by eating raw or insufficiently cooked infected beef or pork.  LIFE CYCLE  Eating raw or insufficiently cooked beef or pork infected with the larva stage of the Tape Worm – Cysticercus or Metacestode or Bladder Worm or Cysticercus Cellulosae or Larvae Taenia.  After swallowing, the larva develops into an adult worm and live in the small intestines  Humans are the natural and final hosts and only carriers of adult tape worms.  Adult tape worms grow up to several meters (4 - 8m)  There will be 3 months period from swallowing the larva to the time of egg detection in stool. EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 57 | P a g e  EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 58 | P a g e   EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 59 | P a g e EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 60 | P a g e EPIDEMIOLOGY  Difficult to diagnose  Frequent disease in developing countries due to;  Poor personal hygiene  Poor sanitation,  Lack of adequate meat inspection  Absence of symptoms (Asymptomatic) DISTRIBUTION  The two are found throughout the world  Taenia saginata is rarely found in India  Taenia solium is rare in Muslim countries CLINICAL PRESENTATION Tinea Saginata:  Most carriers are asymptomatic. If the symptoms occur they are usually verge (abdominal pain, nausea, dizziness, headache, weight loss, increased appetite, pruritus ani, passing segments of tape worms called Proglottids. Tinea Solium:  Present with the similar symptoms like above, except for cysticercosis (Tinea Asciatica does not also present with Cysticercosis) DIAGNOSIS  History of eating raw meat.  Passing worm segments in stool  Stool examination (×3 consecutive stool) formal ether microscopy look for eggs/ ova  Tinea stool detection Copro-antigen (Highly Sensitive up to 95%)  Scotch tape technique  PCR  Microscopically - look for eggs  Macroscopically - worm segments EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 61 | P a g e TREATMENT  Praziquantel 25mg/kg OD  Albendazole 15mg/kg/day for 3 days  Niclosamide 2g OD - induces nausea and vomiting (require antiemetics to avoid autoinfection e.g., when Treating T. solium) EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 62 | P a g e 13 CYSTICERCOSIS  Pork tape worm  Cysticercosis – meta-cestode, MODE OF TRANSMISSION Acquired by autoinfection by ingesting eggs of Taenia solium by man and develops into an Onchosphere (larva) form which penetrates the small intestines and gets transferred to various organs such as;  CNS - Brain (mostly frequent)  Muscles  Eyes  Rare organs (Liver, heart, placenta and peritoneum)  When the larva grows in the brain it is called Neurocysticercosis.  EPIDEMIOLOGY  Endemic in most countries in Africa (Zambia also), Latin America and some parts of Europe and Asia.  CLINICAL PRESENTATION  Depends on the location or site of the parasites  1) Neurocysticercosis  Involving the Brain Parenchyma, Ventricles or Meninges. a) Parenchymal cysticercosis and patients present with;  Epilepsy (Commonest cause of Acquired Epilepsy in Developing Countries)  Mental disturbance  Focal neurology  Tumour-like picture b) Ventricular cysticercosis (subacute picture of hydrocephalus) c) Meningeal cysticercosis (Most severe) which may present as Vascular Headache, Mental Deterioration, Intracranial HTN and Gait Disturbances. EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 63 | P a g e 2) Muscle cysticercosis  Usually asymptomatic  Subcutaneous nodules  Pseudo-hypertrophy of muscles. 3) Ocular cysticercosis  Visual disturbance (use Fundoscopy) Symptoms Extraocular or Intraocular involvement  Periocular swelling/ edema  Proptosis  Ptosis  Ocular pain  Diplopia  Strabismus DIAGNOSIS  Depends on Neuroimaging (MRI superior to CT scan)  Serology - Ag  CSF analysis Ag or Ab detection  Skull X-Ray (shows calcified cysts in the skull)  Radiologic imaging of the muscles (shoulder and thighs)  Stereo-tactic brain biopsy TREATMENT  Chemotherapy  Praziquantel 50mg/kg/day for 2 weeks OR  Albendazole 15mg/kg/day for 2 weeks  Surgical intervention if there’s therapeutic failure  Vitrectomy  Conservative management with chemotherapy (Give Anti-convulsants such as phenobarbitone) EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 64 | P a g e 14 STROGYLOIDIASIS  Causative agent: Strogyloides stercoralis a nematode/round worm,  Aka Thread worm MODE OF TRANSMISSION  Percutaneous penetration of the skin by L3 (Filariform larva)  Oral route - Ingestion of L3 larva  Autoinfection - Internal happens in the intestines (L3 larva) and external in the Perianal area. LIFE CYCLE  Infection starts by skin penetration by L3 larva or ingestion of the L3 larva.  Penetration of the skin and being carried via circulation or lymphatics to the heart the to the lungs and from the lungs the L3 larva get through the bronchi → Trachea → larynx→ swallowed in the oesophagus into the small intestines (proximal duodenum) adult worm develops.   The female adult worms will enter the duodenal mucosa and starts laying eggs in the crypts of Lieberkühn and are then hatched into L1 (Rhabditiform Larva) which is passed in stool.   The male adult worms cannot penetrate the mucosa so they’re flashed out in stool.   The female produces eggs without fertilization (parthenogenesis).  The L1 in the soil has a Microbivorous lifestyle and will develop into L2 then L3. The L3 then penetrates the skin and infect man to complete the life cycle (Homogonic cycle) or   The L3 in the soil molts 2 times and becomes L4 then L5 adult worms (male and female) which mate and produce eggs that then hatch to form L1 then L2 and then the infective stage - L3 (Heterogonic cycle – The worms are free living adult worms in the soil and are thus Facultative Parasites)  Autoinfection  It’s either internal or external.  If L3 is swallowed up there is no lung involvement  EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 65 | P a g e EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 66 | P a g e EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 67 | P a g e EPIDEMIOLOGY 80-100 million being infected globally.   CLINICAL FEATURES Most patients have low worm load and may be asymptomatic or exhibit mild cutaneous and abdominal symptoms.  SKIN  When L3 is migrating under the skin it produces serpiginous eruption called Larva currens which are pruritic, raised erythematous lesions. These are Pathognomonic for Strogyloidiasis.  Non-specific urticarial rash which occur in the waist, abdomen, neck of a child and buttocks.  Petechial haemorrhage  Pruritus Ani  Papular rash GIT  Abdominal pain mimicking Peptic Ulcer Disease  Abdominal distension  Nausea and vomiting  Cramping of lower abdomen  Diarrhoea (intermittent or persistent)  Malabsorption,  Necrotizing jejunitis PULMONARY  Pneumonitis  Picture of Loffler’s syndrome OTHER  Anemia  Azotemia EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 68 | P a g e COMPLICATIONS 1. Disseminated strogyloidiasis  Also called hyper infection syndrome and occurs in defective host immunity.  There is large number of L3 larva disseminated throughout the body.  It is associated with high mortality and morbidity.  The L3 larva can be found in the GIT, CNS, peritoneum, liver kidneys etc.  Bacteremia (as L3 larva moves it is accompanies by bacteria) causing septicemia and in turn septic shock.  Meningitis  Patients with immunodeficiency such as organ transplant, lymphoma, and those on long- term corticosteroids are prone to disseminated Strogyloidiasis.  DIAGNOSIS  Stool examination for the L1 and you collect more than 2 consecutive samples and examine the stool using formol-ether concentration.  Baermann Technique - Piece of cloth funnel and put stool on top, close one end of the funnel and put water and examine.  Stool culture (diagnostic choice) by using media such as Harada mori medium.  Serology - for Ab detection  Sputum examination - find L3 larva in Disseminated Strogyloidiasis  Duodenal fluid - String test for the L1  TREATMENT  Treat both asymptomatic and symptomatic patients  Thiabendazole (Was the DOC but has a lot of side effects such as seizures)  Ivermectin (is the drug of choice ) 200mg/kg/day for 1 to 2 days or  Albendazole (400mg OD for 3 – 7 days) or Mebendazole EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 69 | P a g e OTHER INFECTIONS similar to Strogyloidiasis  Animal Strogyloidiasis  Animal Hookworm (Caused by Ankylostoma caninum which infects Dogs and Ankylostoma Brazilienses infects Cats)  The Snake-like rash Infection caused by L3 is called Cutaneous Larva Migrans or Creeping Eruption)  This infection moves slowly under the skin and does not go below the stratum basalis. TREATMENT OF ANIMAL HOOKWORMS  Albendazole (400mg OD for 2 – 5 days) or  Ivermectin 200mg/kg/day for 1 to 2 days or EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 70 | P a g e 15 GIARDIASIS  Causative agent: Giardia lamblia (aka. G. duodenalis or G. intestinalis)  Protozoal infection.  It’s the commonest intestinal protozoa in the world.  First described by Antoine van Leeuwenhoek in 1681  Later described 200 years after, by Alfred Giardia and Vilem Dusan Lambl in 1859.  Giardia lamblia is a flagellated tear drop shaped protozoa which exist in two forms which are trophozoites and cyst.  Trophozoites have 4 sets of posteriorly directed flagellate for movement.  Prominent feature is a ventral disks (sucker) which attaches to intestinal epithelial cells.  MODE OF TRANSMISSION  Transmission is by faecal-oral route - cyst and it occurs in the following;  Contamination of water and food.  Person-person transmission (individuals with poor personal hygiene) or day care centers. Also happens in developing countries.  Animal to human though evidence is limited. EPIDEMIOLOGY  Giardia lamblia is found in developing countries and North America.  LIFE CYCLE  Acquired by ingesting of cyst then goes in small intestines  Cysts undergo excystation in the duodenum to release the trophozoite which then attach to the duodenum wall or villi by the ventral sucker or disk.  The trophozoite then undergoes asexual reproduction by binary fission and it goes on and on until the trophozoites cover the all surface of the intestines and causes malabsorption (proximal intestines)  Some trophozoites undergo encystations (in the distal intestines) to produce cysts which are passed in stool and are responsible for transmission. EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 71 | P a g e  CLINICAL PRESENTATION Ranges from Asymptomatic cyst passers to Acute diarrheal illness to Chronic diarrheal illness with malabsorption.  5-15%-infected persons are asymptomatic  25-50%-Infected will develop diarrheal illness  35-70% - no trace of infection. ACUTE GIARDIASIS  Incubation period is 1-2 weeks  Symptoms may develop first before detection of cysts in stool.  Patients present with Diarrhoea ranging from profuse and watery diarrhea, to greasy and foul smelling but no blood in the diarrhea.  Associated abdominal cramps, blotting and flatulence.  Malaise,  Nausea and anorexia  No vomiting  Belching and weight loss CHRONIC GIARDIASIS  Characterized by malaise, fatigue, diarrheal illness and the stool is usually greasy and foul smelling, weight loss.  Typically you have the return of the Diarrhoea – Chronic Diarrhea  Evidence of malabsorption of Fats, Vitamin A and B12, Proteins, Iron and Lactose  Failure to thrive in children. EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 72 | P a g e DIAGNOSIS  First clinical - history of Prolonged Diarrhoea with weight loss, no blood, no fever, no vomiting, no tenesmus.  Request stool examination wet mount which shows trophozoites and cysts. Stain with Iodine, Trichome, Iron Hematoxylin  Immunological test - Ag or Ab detection.(Ag detection in stool is more sensitive than Ab)  PCR - high sensitivity and specificity  String Test 4-6hours after, do examination for Trophozoites.  Endoscopy-direct visualization and taking biopsy of the duodenum.  Culture can be done. TREATMENT  5 – Nitroimidazole (Metronidazole and Tinidazole or Ornidazole)  Quinacrine (mepacine).  Furazolidone  Paromomycin  Albendazole 400 mg BD for 3 days EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 73 | P a g e EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 74 | P a g e 16 CRYPTOSPORIDIOSIS (MEANING HIDDEN SPORES)  Causative agents:  Cryptosporidium Parvum - affects both man and animals  Cryptosporidium Hominis - affects man only  It is a GIT parasitic opportunistic infection. MODE OF TRANSMISSION  Via Faecal-oral route by ingesting oocyst (infective stage) via;  Person to person transmission  Water-borne  Food-borne  Animal to humans LIFE CYCLE  Said to be monoxenous which means it can be completed in the GIT of the infected host.  The infective stage is the oocyst which is exogenous.  Infection is acquired after ingestion of the oocyst.  Excystation takes place in the upper GI releasing the sporozoites.  Released sporozoites attaches to the apical membrane of enterocytes.  The parasite can also be found in the biliary tract, pancreatic duct, sinuses and respiratory tract.  Sporozoites enter the intestines and get transformed into trophozoites and undergoes asexual reproduction (merogony or schizongony)  Type I Meront = schizont has (6-8 merozoites).  Type I Meront ruptures to release Merozoites which then invade adjacent epithelial cells and undergoes (merogony) to produce Type II meronts (4 merozoites).  Type II meronts rupture and produce female and male gametes (gamonts)  Zygotes develop into oocysts with 4 sporozoites with thin walls.  Thin walled oocysts are responsible for reinfection  Thick walled oocysts are responsible for transmission of infection outside the body, e.g. in the stool, from infected person to another  EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 75 | P a g e    EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 76 | P a g e EPIDEMIOLOGY:  Epidemics forms are water bone and if it happens as an Endemic it’s because of person to person transmission  It is a Zoonosis People at risk:  Children in developing countries and those in day care centers/nursery  Elderly persons  Travelers,   Animal Handlers - Zoonotic contacts (cattle)  Caregivers of patients with infection; includes (nosocomial)  Immunodeficiency e.g. HIV, malnutrition. Risk Factors in developing countries  Exposure to untreated water (addition risk factor)  Contaminated food and   Poor sanitation  Animal Handlers - Zoonotic contacts (cattle)  Immunodeficiency e.g. HIV, malnutrition. Prevalence:  10-15% in USA  30-50% of people with HIV in developing countries had the infection previously  However with the advent of ART there is drastic decline in cryptosporidiosis.  CLINICAL FEATURES: Two major syndromes 1 Immunocompetent person  Acute watery and self-limiting diarrhoea and its accompanied by the following;  GI distress symptoms such as nausea, vomiting, faecal urgency, abdominal cramps and discomfort.  Patient may have low grade fever or no fever.  Diarrhea duration can be 4-12 days and the infection will disappear even without treatment. EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 77 | P a g e 2. Diverse Immunodeficiency  E.g., HIV  IgG deficiency  Defective cell mediated immunity e.g. due to prolonged steroid use and cytotoxic drugs Patients present with;  Protracted and sometimes life threatening diarrhoeal illness until underlying cause of immunodeficiency is resolved.  In these cases, the patients can pass 20litres per day.  Affects about 50% of HIV positive patients with low CD4 count.  30% - Persistent or relapsing diarrhoea  One –third of these patients with diarrhoea will have dehydration or cholera like diarrhoea requiring IV fluids,  One –third - Biliary tract infection - Sclerosing Cholangitis, Cholecystitis, Papillary Stenosis,  15% - Diarrhoea is self-limiting. Differential diagnosis: Non-Bloody watery diarrhoea 1. Cryptosporidiosis 2. Giardiasis 3. Cystoisosporiasis formerly called Isosporiasis 4. Noninvasive bacterial infections e.g. Enterotoxigenic E.coli 5. Viral infection e.g. Norwalk or Rotavirus EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 78 | P a g e LABORATORY DIAGNOSIS 1 Stool examination: FEC - Looking for Oocyst stage of the parasite 2 to 3 consecutive samples are required. Methods used include  Modified ZN stain (No heating) because the parasite is acid –alcohol fast aka Kinyoun acid fast method.  Monoclonal antibody tagged with Fluorescent substance - Direct immunofluorescence antibody test  Auramine-Rhodamine stain or Auramine-Carbofuschin stain.  Serology-looking for Ab (IgG and IgM)  ELISA (Specific IgG, IgM)  PCR TREATMENT  Maintain adequate hydration (IVF)  No effective antimicrobial agent  HAART will lead to resolution of the condition Drugs with some activity; intact immunity with severe diarrhoea:  Paromomycin  Nitazoxanide (most activity)  Clarithromycin  Paromomycin + Azithromycin Mechanism of Diarrhea Due to the following:  Increase in intestinal permeability  Chloride secretion  Malabsorption Mainly as a result of host immune response to infection EDITED BY: CLINTON SIMWAMBI CIS 2024 UPDATE MBS 600 COURTESY: (MWANZA ALI, GABRIEL MATTHEW NJOBVU AND STEPHEN NYIRENDA) 79 | P a g e 17 CYSTOISOSPORIASIS  Causative agent: Cystoisospora belli  It’s a gastrointestinal tract opportunistic protozoal infection. MODE OF TRANSMISSION By faecal-oral route by ingesting the Oocyst through;  Contaminated food and water  Person to person transmission LIFE CYCLE  Infection is acquired by ingesting the Oocyst.  Mature oocyst has 2 Sporocysts with each Sporocyst having 4 Sporozoites.  Sporozoites are released in the small intestine and undergo asexual reproduction producing merozoites and there is male and female production of the gametes then formation of immature oocysts (containing sporoblasts). Each sporoblast change to sporocyst and development of four sporozoites. EPIDEMIOLOGY  Relatively common and treatable cause of persistent diarrhea  Commonly reported from tropical and sub-tropical region.  Prevalence is unknown  But it is a cause of persistent or chronic diarrhoea in patients with HIV/AIDS and about 15-20% of individuals.  It also causes acute and persi