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434 Cards in this Set
- Front
- Back
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What is the pork tapeworm?
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Taenia solium
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What is the beef tapeworm?
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Taenia saginata
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What is the hydatid?
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Echinococcus granulosus
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What is the fish tapeworm?
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Diphyllobothrium latum
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What is Diphyllobothrium latum?
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Fish tapeworm
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What is Taenia solium?
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Pork tapeworm
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What is Echinococcus granulosus?
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Hydatid
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What is Taenia saginata?
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Beef tapeworm
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What are the characteristics of cestodes and tapeworms?
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No free-living representatives
No gut Depend solely on their tegument to obtain food Hermaphroditic Have a prominent head or scolex Usually the adult worms parasitize the intestine |
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What are the lengths of pork and beef tapeworms?
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Taenia Solium - Pork tapeworm - 1-7 meters long
Taenia Saginata - Beef tapeworm - 5-25 meters long |
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How do Taenia get their name?
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Taenia - latin for ribbon
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What is the geographic distribution of Taeniasis?
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Worldwide, depending on dietary habits and quality of cattle and pork farming
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What is the structure of the proglottid?
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Structure possessing both male and female reproductive elements (testes, uterus, vas deferens, vagins, ovary and *vitellaria*)
Both male and female genital bodies exit the taenia together at a structure called the Genital Pore |
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Taenia Saginata - Scolex and Proglottids
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Taenia Solium - Scolex and Proglottid
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Life Cycle of Taenia from host to man?
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Infection of cattle or pig with larval stage of T. Saginata or T. Solium, respectively.
Oncosphere in blood carried to organs, forms Cysticercus in muscles, brains, eyes and lungs. Cysticercus in muscle is the infective stage. Human ingests meat containing Cysticercus, releasing worm into GI tract. Worm latches on to GI with Scolex, producing infection and releasing many eggs into the feces. |
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What are the features of the Taenia egg?
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Hexacanth - six hooks
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Taeniasis Symptoms?
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GI - Abdominal discomfort, epigastric pain, vomiting. Caused by the physical presence of the worm.
Other organs (cysticercosis) - Cyst formation in brain, eye, lung and liver may cause related symptoms. Due to physical mass and inflammation. |
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How is diagnosis of Taeniasis made?
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Symptoms
History of eating undercooked beef or pork Recovery of Proglottids and/or Eggs in the stool |
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How is the diagnosis of Cysticercosis made?
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CNS and/or symptoms involving other organs
History of ingesting food with T. Solium eggs (or Saginata) Radiographic localization of cysticercal lesions in tissues |
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Treatment for Taeniasis?
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Niclosamide - targets Oxidative Phosphorylation
**Praziquantel - Calcium agonist that leads to tetanic muscular contractions in the worm ~~> Expulsion of the worm, INCLUDING THE SCOLEX |
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Prevention of Taeniasis?
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Veterinary inspection of Beef and Pork
Adequate cooking or freezing of meat - Cysticerci do not survive temperatures below -10 C and above 50 C. |
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Cysticercosis
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Cysticercosis
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Cysticercosis - Brain
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Cysticercosis - Brain
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Cysticercosis
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Scolex of Taenia Saginata
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Taenia Egg
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Taenia Larva Cyst
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Taenia Larvae release
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Taenia Proglottids
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Taenia Solium
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Taenia
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What is the smallest of the Taeniids?
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Echinococcus Granulosus
3-6 mm long |
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What Taeenid has 3 different proglottids, and what are they?
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Echinococcus Granulosus
Immature, Mature, and Gravid |
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Characteristics of Echinococcus Granulosus?
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Smalles of the Taeniids - 3-6 mm long
3 Proglottids - Immature, Mature, and Gravid Hydatid Disease - Liver, Brain |
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What is the geographic distribution of Echinococcus Granulosus?
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Hydatid
Present in Asia, Europe, North, East and South Africa, Parts of Australia and South America, Canada and Alaska. Seldom in the US. Basically everywhere. |
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What is the life cycle of Echinococcus Granulosus?
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Life cycle takes place in 2 different hosts: Intermediate and Definitive
Intermediate host ingests eggs. Larva hatches in intestine, penetrates the intestinal lining and enters the blood stream. Larva distribute to almost any organ, but **LIVER** is most common. The larva develops into a Hydatid Cyst. The DEFINITIVE host is infected when it ingests a Hydatid Cyst. The protoscolex attaches to the host's intestine and develops into a tapeworm. The adult tapeworm is found in the small intestine of the canine (DEFINITIVE HOST). Eggs are then released into the feces. The eggs are ingested by an INTERMEDIATE HOST, and the cycle repeats. |
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What are the two hosts of Echinococcus Granulosus?
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Definitive Host - Canine
Intermediate Host - Human and other warm blooded mammals |
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What are the Sites, Symptoms, and Pathogenesis of Echinococcus Granulosus infections?
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Abdomen - Abdominal Distension, Ascites - Progressively growing cyst
Liver - Obstructive Jaundice - Growing cyst Lung - Pulmonary Abscess, cough, chest pain - Growing cyst CNS - Jacksonian epilepsy - Growing cyst Lung - Fever, pruritus, urticaria, anaphylactoid reactions - Type-1 Hypersensitivity |
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What is the pathology of Hydatid Cysts?
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Caused by Echinococcus Granulosus
***Cyst formation can take 10-20 years Cysts are fluid filled Cysts may reach up to the size of a soccer ball |
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How is the diagnosis of Echinococcus Granulosus made?
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Endemicity
Symptoms X-ray and CT scan Serology Skin (Casoni) Test |
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What is the Casoni Test?
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A simple skin test used for the diagnosis of Hydatid (Echinococcus Granulosus) disease
Sterilized cyst fluid injected subdermally. Wheal response indicates positive response |
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What skin test is used for the diagnosis of Hydatid disease?
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Casoni Test (Echinococcus Granulosus)
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What is the treatment and control of Echinococcus Granulosus infections?
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Surgical removal of the cyst
Injection of 20% hypertonic saline Praziquantel Benzimidazoles (albendazole, mebendazole) - Acts by inhibition of Glucose transport Avoidance of treatment of infected canines |
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How do Benzimidazoles work?
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Inhibition of glucose transport
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How does Praziquantel work?
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Acts as a Ca++ agonist, leading to tetanic muscular contractions of the parasite. Results in paralysis of the worm, and summary expulsion with the scolex
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What is the life cycle of Hymenolepis nana?
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Embryonated egg is released in feces. It is either directly ingested by humans from contaminated food, water or hands, OR the egg is ingested by an insect. Humans and rodents can then be infected by ingesting an infected insect.
Once ingested by a human, the embryonated egg hatches, and a Cysticercoid develops in the intestinal villus. Scolex forms, and the adult lives in the ileal portion of the small intestine. Eggs are released from the genital atrium of the gravid proglottids. Gravid Proglottids can also disintegrate releasing eggs that are passed in stools. Eggs are released in the stool. |
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Characteristics of Hymenolepis nana?
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The Dwarf Worm
Small tapeworm about 40 mm long Adult worm has a retractable rostellum and only one row of hooks (about 20-30) Children harbor the bulk of infections There is very little pathology associated with this infection, unless it is very heavy. |
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What is the treatment for Hymenolepis nana?
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Daily administration of antihelmintic, Niclosamide or Praziquantel, for 4-5 days.
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What is the pathology of Hymenolepis nana?
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There is little pathology associated with this infection unless it is very heavy.
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How is the diagnosis of Hymenolepis nana made?
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Eggs in the feces
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What has 2 Bothria?
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Diphyllobothrium latum (broad fish tapeworm)
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What Taeniid can produce one million eggs per day?
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Diphyllobothrium latum (broad fish tapeworm)
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What are the features of the Diphyllobothrium latum egg?
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Has an Operculum (lid) and a Knob
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What is the geographic distribution of Diphyllobothrium?
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Northern Europe - Diphyllobothrium Latum
North Eastern U.S. - Diphyllobothrium Ursi Northern Canada - Diphyllobothrium Dendriticum |
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What is the life cycle of Diphyllobothrium Latum?
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1) Unembryonated Egg passed in feces
2) Eggs EMBRYONATE in water 3) CORACIDIA hatch from eggs and are ingested by crustaceans 4) PROCERCOID larva in body cavity of crustaceans 5) Crustacean ingested by small feshwater fish, procercoid larva released and develops into PLEROCERCOID larva 6) Predator fish eats smaller infected fish 7) Human eats infected fish 8) Adult develops in small intestine, and releases UNEMBRYONATED eggs in the feces |
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What is the pathology of Diphyllobothriasis?
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Known as "Jewish housewife's disease" because the preparers of gefillte fish or fish balls tended to taste these dishes before theyw ere fully cooked.
Non-specific symptoms - abdominal distention, flatulence, intermittent abdominal cramping, and diarrhea with onset about 10 days after consumption of raw or insufficiently cooked fish. Anemia related to a vitamin B12 deficiency. |
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What is Jewish housewife's disease?
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Diphyllobothriasis - associated with gefillte fish or fish balls
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How is diagnosis of Diphyllobothriasis made?
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Finding eggs in the patient's feces on microscopical examination
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What is the treatment for Diphyllobothriasis?
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Niclosamide, Praziquantel
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How is the spread of Diphyllobothriasis controlled?
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Cooking fish thoroughly, and freezing for at least 12 hours at -12 C or below
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What are the characteristics of Entamoeba Histolytica?
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Enteric Amoeba that Lyses tissues
Movement in host by extending pseudopodia Engulf and digest bacteria and RBC Excrete toxic products that lyse host cells. |
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What is the epidemoiology of Entamoeba Histolytica?
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10% of all humasn are infected by Entamoeba species, and 50 million develop clinical amoebiasis annually, with 40,000-110,000 deaths
Entamoeba Histolytica is implicated in 2.8% of water-borne parasitic disease outbreaks Amoebiasis ranks second (malaria is first) as a cause of death due to parasites |
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What is the source of infection of Entamoeba Histolytica?
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Contaminated water is the source of infection
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What are the trends of Amoebiasis cases in Mexico and the West bank/Gaza?
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Mexico: 1999 - 1.5 million, 2006 - 660,000
West Bank/Gaza: 1999 - 6,500, 2003 - 10,000 |
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What is the life cycle of Entamoeba Histolytica?
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Cysts are ingested with food or water contaminated with human fecal material.
Cysts "excyst" in the small intestine, and the resulting trophozoites colonize the large intestine Trophozoites reproduce by simple division, and they may invadethe lining of the large intestine resulting in symptoms (colitis, diarrhea, dysentary). Cysts are then passed in feces and the cycle repeats Upon invading the lining of the GI large intestine, trophozoites may invade the blood vessels and be transported to other organs of the body |
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What are the virulence factors of Entamoeba Histolytica?
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Binding
Killing Digestion |
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What is the important adherence molecule for Entamoeba Histolytica?
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Gal-Lectin
A 260 kDa Gal/GalNAc specific lectin complex Under reproducing conditions, this heavy complex dissociates into Heavy Subunit and Light Subunit 3 genes encoding the light subunit, lgl 1, lgl 2, lgl 3 |
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What are Amoebapores?
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A family of small amphipathic peptides capable of
insertion into bacterial or eukaryotic membranes and causing cellular lysis They are REQUIRED for virulence |
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What is the role of Cystein Proteinases in Entaemoeba Histolytica?
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Degradation of Human IgA
Disruption of Immune IgG |
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What is the Entamoeba two species hypothesis?
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Proposed by Emile Brumpt - There are two morphologically indistinguishable species: Entamoeba Histolytica and Entamoeba Dispar. Only one of them (Histolytica) causes disease while the other is benign
This theory was entirely discounted and ridiculed Recent molecular data has revived the two species hypothesis We now know that most people are infected with the apathogenic Entamoeba Dispar |
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What is species is identical morphologically to E. histolytica and non-pathogenic?
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Entamoeba Dispar
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What are the characteristics of E. histolytic and E. dispar?
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E. dispar:
In vitro culture - Xenic ConA Agglutination - negative Complement Resistance - negative Zymodemes (isoenzymes) - I & III Entamoeba histolytica: In vitro culture - Axenic ConA Agglutination - positive Complement Resistance - positive Zymodemes (isoenzymes) - II Numerous DNA Sequence differences ~> PCR. 2.2% sequence diversity |
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What is the gentic evidence fo the two species hypothesis?
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Species specific isoenzyme pattern
Multiple antibodies specific for either the pathogenic or apathogenic species Numerous genes sequences showing clear differences Repetitive DNA elements are different Genomic organizaiton of conserved gene loci like actin is different Ribosomal RNA (2.2% differences) |
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How is the diagnosis of E. histolytica made?
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Examination for trophozoites in fluid feces
Examination for cysts in formed feces Scraping and biopsies obtained through a sigmoidoscope Liver abscess aspirates Serology Identification of Entamoeba histolytica / Entamoeba dispar ~> monoclonal antibodies against Entamoeba histolytica galactose adhesin PCR |
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What is the treatment and prevention for E. histolytica?
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Treatment:
Iodoquinol Metronidazole Prevention: Better hygiene Efficient sewage treatment and disposal |
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What is the drug of choise for amebiasis?
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Metronidazole
For invasive amoebiasis, Metronidazole should be combined with a lumen acting drug as it is not fully effective on luminal stages |
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What is the treatment for invasive amoebiasis?
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Metronidazole is the drug of choice, and should be combined with a lumen acting drug as it is not fully effective on luminal stages
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How does Metronidazole work?
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It is a prodrug which is activated by an enzyme (pyruvate ferredoxin oxioreductase) involved in the microaerobic fermentation metabolism of Entamoeba histolytica
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What is the most common flagellate in the human digestive tract?
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Giardia Lamblia
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What are the characteristics of G. lamblia?
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Giardia Lamblia
Most common flagellate in human digestive tract Highly contagious No mitochondria No endoplasmic reticulum No golgi apparatus No lysosomes Reproduction by simple division Glucose as a main food source Aerotolerant anaerobes Classic "Smiley Face" of nucleus (eyes), median body (smile) |
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What is the pathology of Giardia lamblia?
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Asymptomatic carriers
Diarrhea, dehydration, abdominal pain and weight loss No blood loss associated with the diarrhea The disease is not generally fatal Strains of variable virulence |
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How is the diagnosis of G. lamblia made?
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Giardia lamblia
Giardia cysts in the stool Detection of salivary IgA antibodies to Giardia |
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What is the treatment for G. lamblia?
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Metronidazole
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What is the life cycle of G. lamblia?
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Cysts ingested with contaminated water or food.
Cysts "excyst" and trophozoites colonize the small intestine. Cysts passed in feces, and can either enter the reservoir host (beavers) or directly back to human infection |
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Chronic Amoebiasis - mucosal erosion and crater formation
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Chronic Amoebiasis - mucosal erosion and crater formation
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Echinococcus Granulosus
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Echinococcus Granulosus
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Echinococcus Granulosus
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Echinococcus Granulosus
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Echinococcus Granulosus - Cysts
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Diphyllobothrium latum - Egg - Has Operculum (Lid) at top and Knob at bottom
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Diphyllobothrium Latum - Egg
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Diphyllobothrium latum - Proglottid
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Diphyllobothrium latum
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Echinococcus Granulosus - Egg
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Echinococcus Granulosus - Protoscoleces (Hydatid Sand)
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Echinococcus Granulosus
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Entamoeba Histolytica - Cyst.jpg
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Entamoeba Histolytica - Human colon mucosal damage
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Entamoeba Histolytica
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Giardia lamblia
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Giardia lamblia
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Giardia lamblia - Cyst - 12x8 micrometers
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Giardia Lamblia
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Hymenolepis nana (dwarf worm)
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Hymenolepis nana (dwarf worm)
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Trophozoite
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Trophozoites start to engulf detached epithelial cells
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Entamoeba Histolytica - Immature Cyst
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What are the characteristics of Trematoda?
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Flukes or leaf-shaped
Size - few mm to over several cm in length Flat dorso-ventrally Powerful muscular sucking discs for attachment and also spines and hooks as armature Most of their anatomy is composed of reproductive structures Most of them being HERMAPHRODITIC and having complex life cycles They have a ***Simple Digestive Tract*** Molluscs are used as intermediate hosts for their larval forms Targets: blood, lung, liver and intestine of people |
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What are the medically important trematode?
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Schistosoma
Fasciola Clonorchis Paragonimus |
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What are the Schistosoma that cause infections?
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Schistosoma mansonia
Schistosoma haematobium Schistosoma japonicum (Katayama fever) |
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What is the distribution of Schistosoma disease?
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Nearly all of Africa
Parts of southeast Asia Parts of northwest South America 1,000,000 deaths per year |
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What are the characteristics of Schistosoma?
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*Unusual trematodes in that the sexes are separate
They reside in the blood vessels of the definitive host |
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What is the life cycle of Schistosoma?
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Cercaria penetrate teh skin of humans in infected waters.
Maturation occurs in liver circulation They then grow in either the intestines or bladder, releasing eggs into the feces and urine, respectively. Egg releases a MIRACIDIUM, which then infects the intermediate host, the ***SNAIL*** The miracidium then forms a sporocyst, and is released as a Cercaria into the water, which can reinfect humans. |
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What is the intermediate host of Schistosoma?
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Snails
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What are the proteins involved in Schistosoma Cercaria invasion of humans kin?
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Group of proteins involved in calcium binding, calcium regulation, and calcium-activate functions
Two proteins (paramyosin and SPO-1) implicated in immune evasion Protease isoforms implicated in degradation of host skin barriers |
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Where are the male and female Schistosoma located?
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Female exists in the groove (Gynaecophoric canal) of the male
Males are shorter and wider Females are longer and narrower |
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What are the features of the Schistosoma eggs?
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***Presence of a SPINE
Presence of a thin transparent shell Eggs measure between 110-175 by 45-70 micrometers |
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What are the sites of symptoms of Schistosomiasis, and what is their pathogenesis??
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Skin - Dermatitis (swimmer's itch) - Parasitic toxic material, skin damage
GI (mansoni & japonicum) - Abdominal pain, ascites, diarrhea, bloody stool, Fever - Inflammatory response to eggs (mucosal fibrosis) Urogenital (haematobium) - Chronic cystitis and urethritis, fever - Granulomatous fibrosis due to egg-deposits |
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How is the diagnosis of Schistosomiasis made?
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Journey in an endemic region with bath in the local rivers or exposure to contaminated water
Identification of the eggs in feces or urine Immunological methods |
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What is the treatment for Schistosomiasis?
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Praziquantel (biltricide)
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How does Schistosoma accomplish immune evasion?
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The outer membrane of the cercaria has a lipid bilayer and a glycocalyx coat
3 hours after penetration, the outer membrane of the cercaria is replaced by a double lipid bilayer with no glycocalyx coat Components of the host system incorporated into schistosome surface - blood group ags A, B, Lewis X & H factors, MHC antigens |
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How does Schistosoma mansoni evade the complement?
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Produces an analog of decay accelerating factor in order to inhibit C3 convertase
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What species produces an analog of decay accelerating factor in order to inhibit C3 convertase?
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Schistosoma mansoni
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How does the Schistosome accomplish immune deviation?
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Production of a morphine-like substance that down-regulates macrophages, B-cells, T-cells, and NK cells
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How does the Schistosome accomplish active molecular mimicry?
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Passive transmission of genes
Virus mediate transfer - presence of HIV-1 genes in Schistotoma |
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What is the life cycle of Fasciola?
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Unembryonated eggs are passed in feces of humans or pigs into the water
Embryonated eggs form in water Embyonated egg hatches, releaseing Miracidia Miracidia penetrates snail In snail tissue: Miracidia ~> Sporocysts ~> Rediae ~> Cercariae Cercariae released free-swimming into the water Metacercariae on water plant ingested by humans or pigs, causing infection Excyst in the duodenum, and adults in the small intestine, begin producing eggs |
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How is the diagnosis of F. buski made?
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Fasciolopsis buski
Most infections are light and asymptomatic. In heavier infections, symptoms include diarrhea, abdominal pain, and fever History of eating uncooked chestnuts in endemic area Eggs in stool |
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What food is F. buksi infection associated with?
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Uncooked chestnuts
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What infection is associated with ingestion of uncooked chestnuts?
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Fasciolopsis buski
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What is the treatment and control of F. buksi?
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Praziquantel is effective
Avoid eating uncooked chestnuts in endemic areas Sanitary disposal of sewage Elimination of snails |
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What is the geographic distribution of C. sinensis?
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Chlonorchis sinensis
Parts of Eastern Europe Parts of Northeast Asia Parts of Southwest Asia and Japan |
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What is the life cycle of C. sinensis?
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Embryonated eggs are passed in the feces
Eggs are ingested by the snail Inside the snail: ~> Miracidia ~> Sporocysts ~> Rediae ~> Cercariae Free-swimming cercariae encyst in the skin or flesh of fresh water fish Metacercariae in flesh or skin of fresh water fish are ingested by human host Excyst in duodenum, and adults in the BILIARY DUCT. Adults produce eggs, and embryonated eggs are released in the feces |
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What are the symptoms of C. sinensis?
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Chlonorchis sinensis
Epigastric pain Indigestion Liver necrosis and tenderness Liver dysfunctions related to fluke burden Diarrhea, hepatomegaly, jaundice and ascites in heavier infections |
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How is the diagnosis of C. sinensis made?
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Chlonorchis sinensis
Symptoms History of eating improperly cooked fish in endemic area Eggs in stool |
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What food is C. sinensis infection associated with?
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Chlonorchis sinensis
Improperly cooked fish |
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What is the treatment and control of C. sinensis?
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Chlonorchis sinensis
Praziquantel Avoid eating improperly cooked fish in endemic areas Sanitary disposal of sewage Elimination of snails |
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What is the geographic distribution of P. Westermani
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Paragonimus westermani
Small pockets in Central America Small pockets in Western South America Small pockets in Africa Largest affected area in East Asia |
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What are the symptoms of P. westermani infection?
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Paragonimus Westermani
Dry cough, pleurisy Pulmonary pain Blood-stained rusty brown sputum Fluke may migrate to brain, produce eggs and cause epilepsy-like symptoms |
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What food is P. westermani infection associated with?
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Paragonimus Westermani
Improperly cooked crab-meat |
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What pathogen is associated with eating improperly cooked crab meat?
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Paragonimus Westermani
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How is the diagnosis of P. westermani made?
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Symptoms
History of eating improperly cooked crab meat in endemic areas Eggs in sputum |
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What is the treatment for P. westermani?
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Paragonimus Westermani
Praziquantel Bithionol as alternative drug |
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Which Trematode releases its eggs in human urine?
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Schistosoma hematobium
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Which Trematodes release their eggs in human feces?
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Schistosoma mansoni
Schistosoma japonicum Fasciolopsis buski Chlonorchis sinensis |
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What is the drug of choice for all Trematodes?
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Praziquantel
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Chlonorchis sinensis
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Chlonorchis sinensis
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Fasciolopsis buski
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Paragonimus Westermani
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Paragonimus Westermani
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Schistosoma
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Schistosoma - Emission of Cercaria
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Schistosoma - Exit of Miracidium from egg
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Schistosoma haemotobium - Egg
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Schistosoma Japonicum - Egg
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Schistosoma Mansoni - Egg
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Schistosoma
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What are the characteristics of T. vaginalis?
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Trichomonas vaginalis
Four flagella single nucleus |
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What pathogen has four flagella and a single nucleus?
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Trichomonas vaginalis
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How does T. vaginalis multiply?
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Trichomonas vaginalis multiplies by longitudinal binary fission
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How is T. vaginalis spread?
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Via sexual intercourse
Trichomonas vaginalis is present in vaginal and prostatic secretions and urine. It may exist in the vagina or orifice of urethra |
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What is the epidemiology of T. vaginalis?
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Trichomonas vaginalis has a worldwide distribution
Incidence as low as 5% in normal females and as high as 70% among prostitutes and prison inmates U.S. about 3 million people are infected every year |
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What are the symptoms of T. vaginalis infection?
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Trichomonas vaginalis infection is rarely symptomatic in men, although it may cause mild urethritis or occasionally prostatitis
In women, it is often asymptomatic, but heavy infections in a high pH environment may cause mild to severe vaginitis with copious foul-smelling yellowish, sometimes frothy discharge |
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How is T. vaginalis diagnosed?
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Trichomonas vaginalis is diagnosed by Pap stain / microscopy
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What is the treatment for T. vaginalis infection?
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Metronidazole
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What organism can live within T. vaginalis?
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Mycoplasma hominis can survive intracellularly in Trichomonas vaginalis
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In what organism can Mycoplasma hominis live intracellularly in
|
Mycoplasma hominis can survive intracellularly in Trichomonas vaginalis
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What are the infective and diagnostic stages of T. vaginalis infection?
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Infective - Trophozoite in vagina or orifice of urethra
Diagnostic - Trophozoite in vaginal and prostatic secretions and urine |
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Trichomonas infection of the cervix
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Trichomonas vaginalis - Four Flagella, Single Nucleus
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Trichomonas vaginalis - Four Flagella, Single Nucleus
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Trichomonas Vaginalis - Pap stain and microscopy
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Trichomonas vaginalis
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What are the coccidia parasites?
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Cryptosporidium
Isospora, Sarcocystis, Cyclospora Toxoplasma Plasmodium |
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What are the characteristics of C. parvum?
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Cryptosporidium parvum
Major cause of epidemic diarrhea Animal reservoir Severe diarrhea and invasive infection in AIDS patients |
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What is the life cycle of C. parvum?
|
Cryptosporidium parvum
Thick-walled oocyst (sporulated) exits the host Contamination of water and food with oocysts Thick-walled oocyst ingested by the host Inside host, complex sexual and asexual lifecycle takes place. Thick-walled oocysts (sporulated) exit host in feces |
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How is the diagnosis of C. parvum made?
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Cryptosporidium parvum
Detectionof oocysts (4-5 um) in fresh stool samples Ziehl stain |
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What organism is the Ziehl stain used for?
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Cryptosporidium parvum
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What stain is used to detect C. parvum?
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Ziehl stain
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What is the treatment and control for C. parvum?
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Spiramycine, and supportive therapy may be temporarily effective
Control - water quality |
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Cryptosporidium parvum - Oocysts
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What pathogens cause the cutaneous form of Leishmaniasis?
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Leishmania tropica
Leishmania major Leishmania mexicana |
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What pathogens cause the mucocutaneous form of Leishmaniasis?
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Leishmania braziliensis
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What pathogens cause the visceral form of Leishmaniasis?
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Leishmania donovani (India)
Leishmania infantum (Mediterranean form of kala azar) |
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What is the name for the cutaneous form of Leishmaniasis?
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Oriental sore
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What is Oriental sore?
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The cutaneous form of Leishmaniasis
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What is Kala azar?
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The visceral form of Leishmaniasis
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What is the geographic distribution of Leishmaniasis?
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South America (mucocutaneous mainly)
Parts of Africa, Mediterranean, and Asia with all 3 types |
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How many cases of Leishmaniasis are there per year?
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2 million new cases per year
2/3 are Cutaneous Leishmaniasis (CL) 1/3 are Visceral Leishmaniasis (VL) |
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What is the insect vector of Leishmaniasis?
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Sand Fly
Old World Phlebotomus sp. Sergentomya sp. New World Lutzomyia sp. Brumptomya sp. |
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What is the life cycle of Leishmaniasis?
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The vector (a sand fly) ingests macrophages when it ingests blood.
The amastigotes are released in the vector's gut, and the parasite reproduces as promastigotes The vertebrate host is infected with promastigotes when bitten by the vector The promastigotes enter circulating macrophages and reproduce as asmastigotes The macrophage dies, and the amastigotes are released, and they infect more circulating or fixed macrophages The vector (sand fly) ingests the infected macrophages during a blood meal, repeating the cycle |
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What is the morphology of Leishmania?
|
Promastigote (leptomonad) - seen in sand fly
Amastigote (leishmania) - seen in the mammalian host (LD body - Leishman-Donovan body) |
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What is a Kinetoplast?
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A disk-shaped mass of circular DNA inside a large mitochondria that contains many copies of the mitochondrial genome.
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Where are the rRNA and structural genes located on the Kinetoplast?
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The maxicircles
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What is located on the maxicircles of kinetoplasts?
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rRNA and structural genes like cytochrome oxidase subunits I, II, and II, cytochrome b
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What is the progression and resolution of Old World CL?
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CL - Cutaneous Leishmaniasis
Leishmania Major and Leishmania Tropica Caues a moist, cutaneous, ulcer-like lesion at the site of the bite. It starts as a papule that runs an acute course of 1-3 weeks. Natural healing of the infection over 2-12 months |
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What is the vector and reservoir of old world CL?
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CL - Cutaneous Leishmaniasis
Transmission via sand fly Reservoirs - gerbil, rodents, dogs Human to human transmission possible Direct transmission from human to human ~~> primitive form of vaccination |
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What is the progression and resolution of New World CL, and where and among whom is it found?
|
CL - Cutaneous Leishmaniasis
Leishmania mexicana Ulcer usually heals spontaneously over a few months. When bite occurs on ear it results in chronic lesions known as chiclero's ulcer. Because cartilidge of ear is poorly vascularized, immune response is weak, and 40% of cases result in mutilation of ear. Rural diseases that are more prevalent among males who work in forests. Found principally in Central America and Mexico where it occurs in the forest dwelling people who harvest latex from the chicle trees to be used in the manufacture of chewing gum |
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What is Chiclero's Ulcer?
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Chronic lesions on the ear of New World Cutaneous Leishmaniasis
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How is the diagnosis of CL made?
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Diagnosis of cutaneous leishmaniasis is made by using scraping from the edge of the ulcer smeared on a slide, stained and examined microscopically for **amastigotes**
PCR amplification of parasite genes. Tissue biopsies are touched to filters, and filters are hybridized with labeled probes against parasite genes |
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What is the treatment and control for cutaneous leishmaniasis?
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Pentavalent antimonials may be used, such as Stilbophen, Pentostam, or Glucantime. Usually they are not necessary.
Local antibiotic to avoid secondary infection Control: 1) Cover sores 2) Remove reservoirs 3) Remove vectors near habitation using insecticides 4) Screen against sandflies and use repellents |
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Where does mucocutaneous leishmaniasis occur?
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Only in the New World
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What is the progression of mucocutaneous leishmaniasis?
|
Begins like cutaneous leishmaniasis, and the ulcer heals spontaneously within 6-15 months. However, there is **metastatic** spread of the promastigotes from the site of the bite via the lymphatics
Leishmania brailiensis: Metastatic lesion involves the nasal and buccal mucosa causing destruction and malformations of the cartilage and soft tissues Death may occur from secondary infections or respiratory complications |
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What is the reservoir for L. braziliensis
|
Leishmania braziliensis - Mucocutaneous Leishmaniasis
Sloths and Anteaters |
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How is the diagnosis of Mucocutaneous Leishmaniasis made?
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Diagnosis made by using scrapings fromt he edge of the ulcer smeared on a slide, which is stained and microscopically examined for amastigotes
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What is the treatment for mucocutaneous leishmaniasis?
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Treatment is usually ineffective despite intramuscular or intravenous injections of pentavalent antimonials.
Secondary bacterial infections are treated with antibiotics. Liposomal amphotericin B 3mg/kg |
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What causes Kala Azar?
|
Leishmania donovani - found in India
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What is the pathology of Kala Azar?
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Leishmania donovani
This is a metastatic disease Rarely is a lesion seen at the site of bite, and parasites are only occasionally seen in blood, but are present in the spleen and lymph nodes Incubation period of 1-4 months Disease is characterized by fever, anemia, splenomegaly, wasting, imbalance of serum proteins (A/G ratio is reversed) and hyperpigmentation of the skin. The death rate is VERY HIGH if left untreated. |
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Splenomegaly, hyperpigmentation, reversal of A/G ratio of serum proteins and endemicity in India is indicative of...?
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Visceral Leishmaniasis (Kala Azar)
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What is the reservoir of Visceral Leishmaniasis?
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There is no reservoir
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What are the symptoms of Visceral Leishmaniasis?
|
1-4 months: fever, chills, diarrhea, dysentery
Progressive hepatosplenomegaly Skin hyperpigmentation Death, if untreated |
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What pathogen causes the Mediterranean form of Kala Azar?
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Leishmania infantum
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What is the natural reservoir for Mediterranean Kala Azar?
|
Dogs, jackals and foxes
Humans are accidental hosts Principally occurs in children, but unknown why this is the case |
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L infantum causes what?
|
Mediterranean form of Visceral Leishmaniasis (Kala Azar)
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What is the treatment for visceral leishmaniasis?
|
Sodium stibogluconate or pentastam, a derivative antimony
Severe reactions including death occur in 10% of those treated It is very expensive, and the recommended one month treatment costs around $150 Drug resistance has also developed. Up to 70% of infected patients in India are resistant to the drug. Pentamidine isethionate has been used in antimony-resistant visceral leishmaniasis, but although the initial response is often good, the relapse rate is high and it is associated with serious side effects Recently, new drug ***Miltefosine*** developed. Acts as a membrane signaling pathway inhibitor. Taken orally, 95% cure rate. |
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What new drug is in clinical trials for treatment of Leishmaniasis with promising results?
|
Miltefosine - A membrane signaling pathway inhibitor
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Where in the host do Leishmania reside?
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Inside macrophages
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What are the virulence factors of Leishmania?
|
Trypanothione - Resistance to superoxide anion (oxidative burst)
Lipophosphoglycan (LPG) - In the insect vector, LPG: 1) Inhibits the release of midgut proteases in the fly 2) LPG mediates the attachment of promastigotes to the gut wall In the mammalian host: 1) A direct measurement of oxidative burst in stimulated macrophages showed that LPG inhibited this activity 2) LPG inhibits the induction of the burst gp63 - Major surface glycoprotein of L. major promastigotes. It is a GPI-anchored zinc metalloprotease. The gp63 protein appears to mimic fibronectin. The gp63 protein can also degrade lysosomal enzymes. The A2 gene in L. donovani and L. major |
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What is the A2 gene?
|
Leishmania donovani and Lieshmania major
A2 gene familly exists in amastigote stage in L. donovani. In L. major, only a pseudogene A2 genes are tanden repeated with a distinct gene family termed the A2erl genes. A2rel is expressed at equal levels in the promastigote and amastigote. L. donovani amastigotes deficient in A2 protein (asRNA, gene k.o.) are attenuated with respect to survival in visceral organs of infected mice. L. major genetically engineered to express A2 produced higher infection levels in the spleen and liver, compared to control L. major. |
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Cutaneous Leishmaniasis - Amastigotes
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Leishmania - Promastigotes
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Leishmania donovani promastigote binding to macrophage
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Macrophage filled with Leishmania Amastigotes
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What is the whip worm?
|
Trichuris Trichiura
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What is the distribution of T. Triciura? How many people are infected?
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Trichuris Trichiura
Temperate and tropical areas 355 million people infected worldwide |
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How is T. Trichiura diagnosed and treated?
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Diagnosis - presence of eggs in feces
Treatment - Adult worms sensitive to Mebendazole and Benzimidazole |
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What are the symptoms of Trichuris Trichiura infections?
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Mild infections are generally asymptomatic
Serious infections can cause blood diarrhea, anemia, and rectal prolapse |
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What is the threadworm?
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Enterobius Vermicularis
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What is the commonest cosmopolitan worm parasite?
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Enterobius Vermicularis
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What are the characteristics of E. vermicularis?
|
The "threadworm", Oxyuris
Commonest of the cosmopolitan worm parasites in man, infecting mostly children. Worm lays eggs which contain an infective larva ready to infect other people. |
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What are the clinical symptoms of E. Vermicularis infection?
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Enterobius Vermicularis
Most infections are light and asymptomatic Heavy infections - abdominal pain, anal pruritus (biting of the female during the night), pallor and dysentery Enterobiasis can cause severe complications - skin lesions, vulvovaginitis in children, appendicitis, peritonitis, **insomnia** |
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How is the diagnosis of Enterobius Vermicularis made?
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Nocturnal observation. The worms come to the outside of the anus during the night, and can be seen as "cottony wisps"
The "Scotch-test anal swab" utilizes a piece of tape that is pressed against the anus at night. The worms stick to the tape, which is then pressed against a microscope slide and viewed directly. |
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What is the treatment of Enterobius Vermicularis?
|
Mebendazole - single dose of 100 mg repeated at least once after an interval of 2 to 4 weeks.
Pyrantel pamoate - single dose of 10 mg/kg repeated after an interval of 2 to 4 weeks. |
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How rapidly does infeciton of Enterobius Vermicularis develop?
|
Infective larvae are already developed 5-6 hours after the laying of the eggs.
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What is the life cycle of Enterobius Vermicularis?
|
Hands, bed clothing, bed linens, floors, drapes, kitchen counters, clothing, school rooms, desk tops, etc. are contaminated with infective eggs.
Humans are infected when the ingest eggs containing infective juveniles. Eggs hatch in small intestine, and male and female worms migrate to the large intestine and reach sexual maturity. Females crawl out of the anus (during night/early morning) and deposit eggs on the perianal skin. At this point, retroinfeciton possible - eggs that remain on perianal skin long enough hatch, and juveniles will crawl back into the anus to mature. Eggs deposited on the perianal skin become infective within six hours, and can then be spread by being deposited on virtually any surface or object. |
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Enterobius Vermicularis - Egg
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Enterobius Vermicularis - Egg
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Enterobius Vermicularis - Female
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Enterobius Vermicularis
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Trichuris Trichiura - Egg
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Trichuris Trichiura
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What are the characteristics of Nematodes?
|
Round worms
Nematodes have remarkable consistency of shape, normally being vermiform, long and slender with pointed ends Sexes are usually separate The outer surface of the nematode is not cellular but cuticular Unlike the Cestodes and Trematodes, the Nematodes have a continuous gut with a separate mouth at one end and an anus at the other |
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Nematode Structures:
C - cuticle Hy - hypodermis n - Dorsal and Ventral nerves Ps - pseudocoelom ll - Lateral line et - Excretory tubule O - ovary Ut - uterus G - gut |
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What are the characteristics of Strongyloides stercoralis?
|
Dwarf worm
180-380 mm long by 14-20 mm wide Common parasite of man in warm countries Presence of free-living stage Females produce eggs parthenogenetically in the upper part of the small intestine |
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What are the sites of symptoms of S. stercoralis infection and their pathogenesis??
|
Strongyloides stercoralis
Skin - Itching and red blotches - Cutaneous invasion and sub-cutaneous migration of larva Pulmonary - Verminous pneumonia - cough, shortness of breath, wheezing, and fever GI Tract - Mid-epigastric pain, nausea, vomiting, diarrhea/constipation, bloody dysentery - Attachment of adult worms and injury to upper intestinal mucosa General - Weight loss and anemia (rare) - Loss of nutrients and blood |
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What does S. stercoralis cause in young children?
|
Strongyloides stercoralis
"Swollen Baby (or belly) syndrome" Young infants develop massive Strongyloides infections. Fatal infection unless rapid treatment is given |
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How is diagnosis of S. stercoralis made?
|
Strongyloides stercoralis larva observed in stool
Immunofluorescent antibody test |
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What is the treatment for Strongyloides stercoralis?
|
Thiabendazole or Ivermectin
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|
What are the characteristics of the hyper-infective mode of S. stercoralis?
|
Strongyloides stercoralis
Patients with asymptomatic chronic infection that become immunocompromised (steroids, surgery, HIV...) develop serious infection Fatality rate as high as 87% Fatality caused by presence of the parasite but also by heavy bacterial infection |
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What is the life cycle of S. stercoralis?
|
Strongyloides stercoralis
Juveniles are released in host feces. Juveniles molt and either produce infective juveniles (filariform larvae) or free-living juveniles (rhabditiform larvae) In the free-living cycle, males and females mate, producing eggs that hatch new juveniles that can become infective. the infective juvenile penetrate the skin of the host, enter the blood stream and migrate to the lungs. From the lungs, they enter the alveoli and are coughed up and swallowed. Juveniles then take up residence in small intestine and mature into parasitic females. Parasitic females embed in intestinal mucosa, and release eggs which hatch in intestine into juveniles that are released in feces. |
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|
What is the definitive host of T. gondii?
|
Toxoplasma gondii
The cat and relatives in the family Felidae |
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|
What symptoms can toxoplasmosis cause?
|
Congenitally infected children may suffer impaired vision (retinitis) and mental retardation (encephalitis)
Immunosuppressed patients may have central nervous system disease (encephalitis) Infection is usually asymptomatic in immunocompetent individuals |
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What is the pathogenesis of toxoplasmosis?
|
Number of factors that determine if infected host will express disease smptoms
Diet - if uncooked or poorly cooked meat is eaten Immunocompromised Host - if the patient is undergoing suppressive immunotherapy as in the case of transplant patients or if the patient is suffering from HIV. **New born infants are particularly susceptible to heavy infections |
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What are the characteristics of congenital toxoplasmosis?
|
Toxoplasma gondii can cause abortion of the fetus or can cause severe malformation at birth
Most authorities believe that if a woman is infected before she is pregnant transplacental transmission will not occur The greatest risk of congenital toxoplasmosis occurs during the first trimester of pregnancy The transmission rate from a maternal infection is about 45%. Of these 60% are sub-clinical infections, 30% have severe damage such as hydrocephalus, intracerebral calcification, retinochoroiditis, and mental retardation, and 9% result in death of the fetus |
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How is the diagnosis of toxoplasmosis made?
|
Serologic testing - ELISA
Pregnant women - Serological tests before or at the beginning of the pregnancy. Survey during pregnancy Immunosuppressed patients - direct diagnosis (PCR) |
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What is the treatment of toxoplasmosis in immunoconversion of a pregnant woman? In immunosuppressed patients? If the fetus is affected?
|
Imunoconversion of a pregnant woman - Spiramycine (Rovamycine) until the childbirth
Immunosuppressed patients - PYRIMETHAMINE (inhibitor of DHFR - dihydroxyfolate reductase) + SULFADIAZINE If the fetus is affected - PYRIMETHAMINE + SULFADIAZINE (sulfonamide) + ACID FOLINIC |
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|
How is toxoplasmosis prevented?
|
Avoidance of contact with cats during pregnancy
Avoidance of eating uncooked or poorly cooked meat |
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What is the life cycle of T. gondii?
|
Toxoplasma gondii
The definitive host is the cat, which releases unsporulated oocysts in its feces. The oocyst then sporulates, and can infect a human directly or an intermediary animal. In the intermediary, pseudocysts form in tissues, which if improperly cooked can be ingested in beef, lamb, pork, etc. The organism enters the host, and the Tachyzoites are ingested by macrophages, where they multiply. The Tachyzoites then migrate to tissues where they form pseudocysts. |
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Nematodes Structures
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Strongyloides stercoralis - Larva
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Strongyloides stercoralis - Larva
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Strongyloides stercoralis
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Toxoplasma gondii - Pseudocyst filled with bradyzoites
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Toxoplasma gondii - Tachyzoites
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|
What is the epidemiology of hookworms?
|
Distributed in the Americas, Africa, Asia, Australia, and parts of Europe.
Hookworms parasitize more then 900 million people worldwide. Cause a daily blood loss of 7 million liters. |
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|
What are the species of hookworms?
|
Ancylostoma duodenale
Necator americanus |
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|
What are the characteristics of hookworms?
|
Hemophages - Change from white to red after a meal
Necator americanus - few, broad dull teeth at the mouth Ancylostoma duodenale - many, sharpy pointy teeth at mouth Male has broad fan-like tail, Female has pointy tail |
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What are the sites of symptoms of hookworms, and what is their pathogenesis?
|
Dermal - Erythema, macules, papules (ground itch) - Cutaneous invasion and sub-cutaneous migration of larva
Pulmonary - Bronchitis, pneumonitis, eosinophilia - Migration of larvae through lung, bronchi, and trachea GI - Anorexia, epigastric pain, and GI hemorrhage - Attachment of adult worms and injury to upper intestinal mucosa Hematologic - Iron deficiency, anemia, hypoproteinemia, edema, cardiac failure - Loss of nutrients and blood |
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|
How is the diagnosis of hookworms made?
|
Travel in an endemic region
Eggs in stool |
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|
What is the treatment and prevention of hookworms?
|
Benzimidazole: Mebendazole, Flubendazole, Albendazole
Pyrantel To correct anemia - Iron and Vitamin B12 1) Hookworm disease is best controlled by sanitation involving proper disposal of human feces 2) Treatment of infected individuals and proper diets to correct anemia 3) Protective measures such as wearing of shoes in areas where hookworm is endemic |
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|
What is the life cycle of hookworms?
|
Eggs hatch in soil, and juveniles develop into infective stage.
Infective juveniles penetrate the skin, and migrate via the blood to the lungs. Juveniles penetrate alveoli and are coughed up and swallowed. Juveniles enter small intestine, attach to surface and mature into adult forms. Adult hookworms attach to lining of small intestine and feed on blood. Females produce eggs that are passed in the host's feces. |
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Hookworm Egg
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Hookworm Egg
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Hookworm Egg
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Hookworm Morphology - Left = Necator americanus - Right = Ancylostoma duodenale
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Hookworms
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|
What is Chagas disease?
|
Trypanosoma cruzi
|
|
|
What is the Epidemiology of Chagas disease?
|
Trypanosoma cruzi
Primarily South and Central America 15-20 million people are infected Transmission associated with poor living conditions |
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|
What is the life cycle of T. cruzi?
|
Trypanosoma cruzi
Trypomastigote infects humans, and distributes in the body. Amastigotes are released in the feces, and then ingested by the vector, the REDUVID bug. Inside midgut Amastigote ~> Epimastigote, which then multiplies and becomes the Metacyclic Trypomastigote (infective stage) |
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|
What is the vector and reservoir for Chagas disease?
|
Trypanosoma cruzi
Vector - Reduvid Bug Reservoir - Armadillo |
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|
How does T. cruzi replicate in the cell of the vertebrate host?
|
Trypanosoma cruzi
Trypomastigote attaches to membrane and initiates signaling process that results in elevation of intracellular Ca++. Lysosomes migrate to trypomastigote attachment site and fuse with membrane. As they fuse, parasite moves into cell in a tight vacuole formed by lysosomal membranes. Lysosome-derived vacuole is disrupted, releasing the parasite into the cytosol. In cytosol, parasite differentiates into amastigotes, which replicate by binary fission, doubling time 12 h. Amastigotes differentiate back into infective trypomastigotes, which release into the blood stream upon rupture of host cell. Bloodstream trypomastigotes can infect new cells, or be ingested by the insect vector (REDUVID bug). |
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|
What are the clinical syndromes of Chagas disease?
|
Asymptomatic - No symptoms at this stage which may last for many years. No trypomastigotes in the bloodstream, but antibody (IgG) against T. cruzi is present
Acute - Site of infection develops localized inflammatory reaction "Chagoma nodule". If infection is on the eye, unilateral edema and conjunctivitis develops, the "CHAGOMA/ROMANA'S sign". Trypanosomes appear in blood in about 10 days. Systemic signs 2-3 weeks after infection, of high feveres, myalgia, CNS may be affected. ***Disease more severe in children <5 years. Chronic - 10-30% of individuals progress from the asymptomatic stage to the chronic stage. There are very low levels of parasites in the blood. The adverse effects of chronic Chagas disease include enlargement and aberrant function of the liver, spleen, heart, esophagus, and large intestine. |
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|
What is Romana's sign?
|
Infection of the eye by Trypanosoma cruzi that results in unilateral edema and conjunctivitis
|
|
|
How is the diagnosis of Chagas disease made?
|
Trypanosoma cruzi
Blood microscopy Low sensitivity during the chronic stage Xenodiagnosis (50% efficiency) Serological detection ELISA - Chagas kit PCR |
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|
What is the treatment and prevention of T. cruzi?
|
Trypanosoma cruzi - Chagas disease
Nifurtimox - decreases duration and severity of the acute phase. But if it is taken orally for long periods, severe side effects - pain, nausea, vomiting, neurologic symptoms. No effect on chronic phase. Benzimidazole - can suppress parasites in the acute phase. This drug is also taken orally for long periods and has many side effects. Avoid and control the insect population. No vaccine. |
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|
What are the antibody based molecular diagnosis kits available for Chagas disease?
|
Trypanosoma cruzi
1) FATALA kit - measures T. cruzi antibodies in blood using 2 recombinant proteins 2) BIO CHAGAS kit - uses cocktail recombinant T. cruzi antigens. Infection sera produces blue precipitate on strip in 60 minutes $25 US per kit |
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|
What are the theorized targets in the THEORETICAL autoimmune mechanism of chronic Chagas disease?
|
Trypanosoma cruzi
B13 - cardia myson Cruzipain - 210 kDa antigen from a skeletal muscle extract Cha - ? |
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|
Trypanosoma cruzi
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|
Trypanosoma cruzi
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Trypanosoma cruzi - In Tissue
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|
Epidemiology of T. spiralis
|
Trichinella spiralis
At one time widely distributed in Europe and US, though reduced now due to livestock maintenance. Found in many species of carnivores and omnivores. Infection related to consumption of raw or undercooked meat, mainly pork. |
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|
Characteristics and morphology of T. spiralis?
|
Trichinella spiralis
1) Smallest Nematode parasite of humans 2) Although it has a single host life cycle, the host acts as both the primary and intermediate host. 3) There are no free-living stages Morphology: Males - 1.5 mm Females 3.4 mm Females (ovoviviparous) produce living young (approximately 1,500 per female over a period of 4 to 16 weeks) and then die. Males die after mating |
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What is the life cycle of T. spiralis?
|
Trichinella spiralis
Humans are infected most often by eating improperly cooked meat products that contain infective juveniles. Carnivores and omnivores are infected when they eat meat containing the infective juvenile stage. Juveniles digested from muscle, and penetrate into tissues of small intestine and grow to sexual maturity. Juvenile worms migrate to muscles of host and mature into infective stage. |
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What diseases does T. spiralis cause in humans?
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Trichinella spiralis
Trichinosis and Trichnellosis |
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What are the symptoms of Trichinosis, and what is their timeline?
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GI - 24-72 hours - Nausea, vomiting, abdominal pain, diarrhea, head ache
Circulation - 10-21 days - Edema, periorbital conjunctivitis, photophobia, fever, chills, sweating, muscle pain, spasm, eosinophilia Myocardium - 10-21 days - Chest pain, tachycardia, edema, vascular thrombosis Brain - 14-28 days - Head ache (supraorbital), vertigo, tinnitus, deafness, mental apathy, delirium, coma, loss of reflexes |
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How is the diagnosis of Trichinosis made?
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Symptoms
Recent history of eating undercooked pork Eosinophilia Increased serum creatinine phosphate and lactage dehydrogenase Serology |
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What is the treatment and prevention of Trichinosis?
|
All the nematocides are efficient against the adult stage (very short phase)
Benzimidazole should be used against L1 stage because of their bood diffusion Prevention: 1) Cook pork thoroughly (also bear, wild pigs) 2) Cook all garbage fed to hogs 3) Proper meat handling, ordinary curing and slating of pork products will not kill encysted juveniles 4) Freezing is effective if carried out properly |
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Trichinella spiralis - Female
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Trichinella spiralis - Infective juvenile in muscle
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Trichinella spiralis - Trichinosis
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What are the types of Trypanosomiasis?
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African trypanosomiasis - Sleeping Sickness
Trypanosoma brucei rhodesinse Trypanosoma brucei gambiense American Trypanosomiasis - Chagas Disease T. cruzi |
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What is the distribution of Sleeping Sickness?
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African trypanosomiasis - Sleeping Sickness
Western, central and southern Africa |
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What is the host, vector, localization and disease of the two strains of African Sleeping Sickness?
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T. brucei rhodesinse:
Host - Human, antilopes, deer Vector - Glossina morsitans Localization - Savannah Disease - acute (weeks-months) T. brucei gambiense: Host - Human Vector - Glossina palpalis Localization - Rivers Disease - Chronic (1-2 years) |
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What is Winterbottom's sign?
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Enlarged neck lymph nodes in Trypanosoma brucei gambiense or Trypanosoma brucei rhodesinse disease
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What is the life cycle of African Sleeping Sickness?
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T. brucei gambiense or T. brucei rhodesinse
Infection of human by bite of TSE-TSE FLY (GLOSSINA). Trypomastigote multplies in blood, lymphnodes and spinal fluid. Trypmastigotes in blood can be re-ingested by the vector. In the vector, multiplication occurs in midgut, then migration to salivary gland. Epimastigote stage in salivary glands, with further multiplication. Transforms to metacyclic trypomastigote in salivary glands, which are infective. |
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What are the forms of T. brucei?
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Trypanosoma brucei
Epimastigote (crithidial form) - in the insect Trypomastigote (trypanosomal form) - in the mammalian host |
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What is the pathology and immunology of T. brucei disease?
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Trypanosoma brucei
Pathology: Inflammation Antigenic change CNS damage by the organisms Immunology: Antibodies are not protective due to antigenic change Polyclonal B cell expansion; hyper-IgM Hypocomplementemia (CRP) Immunosuppression |
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What mediates somnolence in T. brucei disease?
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Somnolence - Indole Catabolites
Toxic metabolites of aromatic ring AAs (Tryptophan, tyrosine, phenylalanine) Anaesthetic affects Damage blood vessels Induce temperature changes Immunosuppression |
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How is the diagnosis of T. brucei made?
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Trypanosoma brucei
History of travel and fly-bite Symptoms Blood smear and/or CSF Anionic supper concentration Bioassay (mouse) Immunoassays |
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What is the treatment and control of T. brucei disease?
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Pentamidine
Arsenical suramin (early phase, inhibits glycolytic enzymes of trypomastigote) Melarsoprol (arsenical) Eflornithine (difluoromethyl-ornithine, ADVANCED DISEASE) No reliable vaccine ~> Antigenic variation Tse-tse fly insecticides or traps with an attractant bait plus insectiside |
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How does antigenic variation in T. brucei occur?
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Possesses a surface coat of proteins, 10 million copies of a single molecular species of antigen
VSG - Variant Surface Glycoprotein - Each trypanosome carries a large repertoire of VSG genes coding for multiple VSG variants with different primary sequence |
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How is the VSG ES organized?
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Variable Surface Glycoprotein Expression Site
20 different ESs Only one is active at any one time Polycystronic transcription followed by mRNA processing Many homologous sequences Rich in recombination events ESs as a whoel are homologues in sequence, further supports recombination Many combinations to build a repertoire of different VSGs and ESAGs. Contributes to host adaptation |
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How is cellular regulation in T. brucei accomplished?
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Greatly unknown
Open chromatin conformaiton in the active ES, closed in the silent ones Base J (a modified uracil) was found incorporated in the silent ESs, while absent from the active one Base J probably represses transcription in a way similar to methylation |
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What is the VSG switching mechanism in T. brucei?
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Gene conversion (homologous recombination) - most common
Mosaic VSG formation VSGs are transcribed in a specialized nuclear compartment |
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Trypanosoma brucei
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Trypanosoma brucei - trypomastigote form
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Trypanosoma brucei - VSGs
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Trypanosoma brucei
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Epidemilogy of Malaria?
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40% World population at risk
300 million develop clinical malaria 1 million die each year - mainly children Generally limited to tropics and subtropics P. Falciparum - Asia, africa, and south and central america P. vivax - less temperature sensitive ~> most widespread Europe (rare), north africa, middle east, southa merica P. ovale - rate, Central and occidental africa P. malariae - Tropical africa, south and central america |
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What are the strains of malaria, and which is the most virulent form?
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Plasmodium species:
P. Falciparum - most virulent P. vivax P. ovale P. malariae |
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How is malaria transmitted?
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Anophele (female mosquito) and also blood transfusion
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What is the life cycle of malaria?
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Mosquito ingests gametocytes, which form zygote in gut and develops into oocyst. Oocyst releases sporozites, which reach salivary gland and are infective.
Mosquito bites again, injecting sporozites into host. Sporozites first infect hepatic cells (can be dormant here), which rupture and release merozoites that infect RBCs. Reproduction in RBCs, and rupture to release gametocytes. |
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What are the symptoms of the three stages of malaria?
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Cold Stage - Fever, shaking chills
Hot Stage - High fever, headache, nausea, vomiting, dizziness, pain, delirium Sweating Stage - Sweating, fall in temperature, prostration Anemia (pallor, tiredness, fatigue, shortness of breath), splenomegaly, hepatomegaly |
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What is cerebral malaria?
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Most often seen with Plasmodium falciparum
Cerebral malaria (CM) collectively involves the clinical manifestations of P. falciparum malaria that induce changes in mental status and coma. It is an acute, widespread disease of the brain which is accompanied by fever. Mortality is 25-50% In untreated person, CM is fatal in 24-72 hours The histopathological hallmark of this encephalopathy is sequestration of cerebral capillaries and venules with parasitized RBCs and and non PRBCs. Ring-like lesions in brain are major characteristics. Disease risk factors include being child under 10 years of age and living in malaria-endemic area. |
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Possible mechanisms to explain CM?
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CM - Cerebral malaria
P. falciparum erythrocyte membrane protein (PfEMP-1) Ligands on endothelial cells, such as ICAM-1 or E-selectin Reduction of microvascular blood flow and induces hypoxia Expression of iNOS, oxidative stress and finally apoptosis in endothelial cells |
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What are the incubation periods, erythrocyte cycle (hr), liver status, and parasitemia (mm^3) of the 4 plasmodium species?
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P. falciparum:
Incubation - 7-10 days Erythrocytic cycle - 48 hours Persistent Liver Stage - No Parasitemia - 50k-500k, max 2.5 mil P. vivax: Incubation - 10-17 days Erythrocytic cycle - 48 hours Persistent Liver Stage - Yes Parasitemia - 20k, max 50k P. malariae: Incubation - 18-40 hours Erythrocytic cycle - 72 hours Persistent Liver Stage - No Parasitemia - 6k, max 20k P. ovale: Incubation - 10-17 days Erythrocytic cycle - 48 hours Persistent Liver Stage - Yes Parasitemia - 9k, max 80k 48 hours - tertian 72 hours - quartan |
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How is diagnosis of malaria made?
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Blood smear with Giemsa stain (methylene blue and eosin) under microscope
PCR - 1 plasmodium in 10 mL of lbood Immune detection |
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What are Schuffner's dots?
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Microscopically visible specs of P. vivas (malaria) under blood smear microscopy with giemsa stain
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What induces gametocyte exflagellation in infected mosquitoes?
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Xanthurenic acid
Additional stimulus: drop in temperature |
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What induces infectivity in P. falciparum containing mosquitoes?
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Xanthurenic acid induces gametocyte exflagellation of plasmodium in the mosquite
Additional stimulus - drop in temperature |
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What are the indirect immune responses of the mosquito to plasmodium proteases?
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Various proteases are secreted from the midgut epithelium. Ingested asexual erythrocytic stage parasites and **any gametocytes that have failed to transform into ookinete stage are also digested**
Two GPI-anchored proteins, P25 and P28, cover the ookinete surface and their disruption results in increased sensitivity to proeases in vitro, and reduced oocyst formation, in spite of normal ookinete numbers. |
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What is the cross interaction between bacteria and plasmodium in the mosquito gut?
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Feeding of gram-negative bacteria with a malaria-infected meal reduces oocyst formtaion
Administration of antibiotics has a positive effect on parasite development - it kills the bacteria and therefore helping the parasite Bacteria DECREASE plasmodium |
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What is the role of humans and mosquitoes in malaria transmission?
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Both humans and mosquitoes are not passive.
Mosquitoes secrete proteases in the gut, and have flora bacteria that both decrease plasmodium infectivity |
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What are the human host defense mechanisms against malaria?
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Antibodies to sporozoites can prevent invasion of hepatocytes
IFN-gamma and cytokines inhibit development of liver stage CD8+ T-cells lyse infected hepatocytes Abs to merozoites can prevent invasion of RBCs Duffy antigen required for invasion of RBC. Sickle cells provide poor environment for P. falciparum Cytokines can destroy infected RBCs Abs to gametocytes, gametes, ookinetes can prevent development of sporozoites |
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What is the development cycle of malaria?
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Sporozites infect humans
Invade hepatocytes, become merozoites Merozoites invade RBCs, become gametocytes Gametocytes ingested by mosquito. Inside mosquito, Gamete ~> Zygote ~> Ookinete ~> Oocyst |
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How does sickle cell anemia protect against malaria?
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Sickling depletes cell reserves of potassium which is required for the parasite to grow
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What is malaria prophylaxis?
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Sleep under netting
Use mosquito repellent Consult an updated map - Chloroquine resistant vs. sensitive malaria Chloroquine In chloroquine resistant areas: Mefloquine Doxycycline Primaquine |
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What are the chemoprophylxis for malaria?
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Chloroquine is the recommended chemoprophylactic for traveling to areas with plasmodia still chloroquine sensitive
In chloroquinine resistant areas: Mefloquine - 50% resistance in Asia. OK for pregnancy. Risk of neuropsychatric side effects (1 in 10k-13k users). Begin 2 weeks before entering and continue 4 weeks after leaving. Doxycycline - Begin 1-2 days before travel and continue for 4 weeks after. Primaquine - Not available in Israel - G6PD (glucose-6-phosphate dehydrogenase) activity is needed. Better for P. vivax (kill hypnozoites). Best combined with cloroquine. |
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What chemoprophylaxis is best for P. vivax?
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Primaquine
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What drug is good for prevention AND treatment of P. falciparum malaria?
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Malarone
2 drugs, atovaquone and proguanil. Works by killing parasites in blood and liver. Useful for individuals who cannot tolerate or take mefloquine Begin 1-2 days before entering malaria zone, and continue for 7 days after leaving. ***Downside - price, significantly more expensive than other antimalarials Dose is one table daily. Not recommended for people who weigh less than 40kg. The commonest side effects are headache, abdominal pain, and diarrhea. ***It does not have neuro-psychiatric effects of mefloquine. Not recommended during pregnancy, nor if you are taking certain drugs. In particular, tetracyclines or a certain anti-nausea drug called metoclopramide. DOES NOT KILL HYPNOZOITES |
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What are the treatments of acute malaria?
|
Tissue schizonticides (liver stage):
Primaquine Blood schizonticides: Chloroquinine sensitive Plasmodia: Chloroquine Chloroquine-resistant Plasmodia: Mefloquine Quinine Quinidine Pyrimethamine-sulfadoxine Doxycycline Halofantrine Artemisinin Malarone |
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What is hemozoin?
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A digestion product of hemoglobin produced by blood eating parasites such as malaria
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How does chloroquine work?
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Inside the plasmodium parasite, it targets the food vacuole.
It blocks transport proteins CRT and MDR1 externally or possibly internally. Inside the vacuole, it blocks digestion of Heme to hemozoin by targetting PfHRP2 (histidine rich protein 2) |
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What drug blocks digestion of heme in plasmodium?
|
Chloroquine
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What antimalarial drug is an antifolate?
|
Pyrimethamine proguanil
Blocks DHFR |
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How does pyrimethamine proguanil prevent malaria?
|
Antifolate, acts by blocking DHFR
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What is Artemisin?
|
Remedy from a nobleman's tomb. Herb wormwood used by Chinese for thousands of years in various remedies.
One use is treatment of malaria, lost until rediscovered in archeological dig in early 70s. Inside tomb of Han nobleman, found silk scroll labeled "medical treatments for 52 diseases", containing 238 treatments including herbla recipe for treatment of malaria by soaking leaves and branches of artemisia herb in water and drinking it. This silk scroll is now the oldest existing text on Chinese medicine. |
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What is Qinghaosu?
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Artemisin derivative used to treat malaria
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What is the geographic distribution of Ascariasis?
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Central and South America, Africa, Asia and Australia
25% of the world's population is infected with this parasite |
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What are the characteristics of Ascaris?
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Very large worms
Head has 3 jaw-like structures oriented on the circumference of the mouth that clamp down Eggs have a bumpy shell |
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What is the unique identifiable feature of Ascaris eggs?
|
A bumpy shell
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What are the characteristics of Eggs of Ascaris?
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Eggs are very resistant to environmental stress
they can survive in moist soil for 3-5 years They are resistant to cold, heat, and to antiseptic In endemic zone until 100 eggs/g of soil |
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What is the life cycle of Ascaris?
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Ascaris Lumbricoides and Ascaris Suum
Eggs are ingested by host and hatch in small intestine. Juveniles penetrate intestine and enter blood stream, where they travel to lungs and molt into third stage juveniles. Third stage juveniles migrate into alveoli, and are "coughed up" and swallowed. Juveniles then complete their development in the small intestine. Adult males and females are in the small intestine, and females produce eggs that are passed in the feces (single female can produce 200,000 eggs per day). Juveniles in eggs mature to infective (second) stage. |
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What are intestinal roundworms?
|
Ascaris Lumbricoides and Ascaris Suum
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What are the symptoms of Ascariasis?
|
Ascaris Lumbricoides
Pulmonary - Cough, wheezing, dyspnea, sub-sternal discomfort Small and large intestine - Abdominal pain, distended abdomen, anorexia, weight loss, occasional vomiting and loose stool, ***Occlusion, acute (and fatal) peritonitis*** |
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How is the diagnosis of Ascariasis made?
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No direct diagnosis during invasive phase. Indirect diagnosis during invasive phase using immunological methods.
Acute phase - presence of eggs in feces X-ray (often observed during non-specific exam) **The worm is sensitive to anesthetics The worm can get out in the feces or during vomiting |
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What is the treatment and prevention for Ascariasis?
|
Infection should always be treated because of risk of complications.
Benzimidazole (mebendazole) Piperazine Pyrantel Pamoate Prevention - Hygiene ~Promiscuous defacation of small children around houses ~Inadequate sanitation ~Use of human night soil as fertilizer |
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What is the anti-inflammatory effect of Ascariasis?
|
Binding of WBC to endothelium selectins is inhibited by lectins secreted by the parasite.
Chemokines destroyed by parasite's proteases. Secretion of serpins inhibits host proteases. NO production and oxidative stress is inhibited by anti-oxidant molecules like GST. |
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Ascariasis - Intestinal Rupture
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Ascariasis - Xray
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Ascaris Lumbricoides
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Ascaris Lumbricoides
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Ascaris Lumbricoides - Egg - BUMPY SHELL
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Ascaris Lumbricoides - Head of adult worm
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Ascaris Lumbricoides - Sensitive to anesthetics.jpg
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Ascaris Lumbricoides
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Cerebral Malaria
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Malaria - human infected cell
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Plasmodium falciparum gametocyte
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Plasmodium falciparum gametocyte
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Plasmodium Oocysts inside mosquito
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What is the Guinea worm?
|
Dracunculus medinensis - one of the largest nematodes known with adults reaching 50-120 cm in size
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What is the epidemiology of the Guinea worm?
|
Dracunculus Medinensis
Distribution - Asia (India, Iran, Pakistan, Afghanistan, Turkestan, USSR), Africa (Nile Valley, Central, East), Indonesia, Fiji, Brazil 50 million people infected worldwide |
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What is the lifecycle of C. medinensis?
|
Dracunculus medinensis - Full life cycle occurs in 3-4 months
Humans are infected when ingesting water containing infected copepods Juvenile worms exit the intestinal tract and migrate to the subcutaneous tissues. Male and females mate, and male dies. Female worms migrate to skin (legs, ankles, feet). Females produce juveniles, and a blister forms under the skin. Blister produces a burning sensation, and when put into water, blister bursts releasing juveniles into the water. Juveniles are ingested by copepods and mature into infective stage, and cycle repeats. |
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What are the symptoms and pathogenesis of D. medinensis?
|
1) Rash accompanied by severe itching, nausaea, vomiting, diarrhea, and dizziness
2) A blister is formed 3) The blister breaks, liberating toxic fluids contained in the blister 4) When this area is exposed to water, the female nematode discharges numerous first stage juveniles into the water (ovoviviparous) |
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What is the prevention and treatment of Guinea worm?
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Water treatment
Mebendazole is effective Worm must be extracted, a few cm a day |
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Dracunculus medinensis
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Dracunculus medinensis
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Dracunculus medinensis
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Dracunculus medinensis
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Dracunculus medinensis
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What are the three causes of Filariasis in humans?
|
Wuchereria bancrofti
Brugia malayi Brugia timori |
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What is the epidemiology of the causative agents of Filariasis?
|
Wuchereria bancrofti - Eastern South America, Sub-saharan Africa, Southeast Asia and Indonesia/Polynesia
Brugia malayi - Southeast Asia and Indonesia/Polynesia Brugia timori - small area of Indonesia/Polynesia 120 million people affected in 73 endemic countries world-wide |
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What is the disease process of Filariasis?
|
1) Entry - larva via mosquito bite
2) Larva mature to adults in lymphatics and produce microfilariae which enter blood 3) Spread of microfilariae 4) DISEASE - Lymphadenitis, Lymphangitis, elephantiasis 5) Exit - microfilariae ingested by mosquito, develop to infective stage |
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What are the characteristics of W. bancrofti?
|
White worm with a smooth cuticle and bluntly round ends
Males - 4cm x 0.1 mm Female - 8cm x 0.2 mm (ovovivipare) |
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What are the four stages of W. bancrofti disease?
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1) Incubation period (3 to 12 months) - no symptoms
2) Acute stage - swelling of extremities, pain, weakness of arms and legs, headache, insomnia. Fever usually not present 3) Period of recovery 4) If there is continued reinfection, the cycle repeats and elephantiasis may result |
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How is diagnosis of W. bancrofti made?
|
Diagnosis is based on history of mosquito bites in endemic areas
Clinical findings Presence of microfilaria in blood samples COLLECTED AT NIGHT Serology - PCR |
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Diagnosis of what organism requires blood samples be collected at night?
|
Wuchereria Bancrofti - Filariasis/Elephantiasis
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What is the management of Filariasis?
|
Wuchereria Bancrofti
1) Antibiotics to prevent secondary infections 2) Pressure bandages to reduce swelling 3) Surgical removal of infected tissues to improve lymph flow 4) Chemotherapy (new) - Diethylcarbamazine, Ivermectine 5) Vector control (malaria, intermediate host) |
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What are Wolbachia?
|
Wolbachia are Gram-negative bacteria that form intracellular inherited infections in many invertebrates.
Wolbachia is related to rickettsial bacteria. It is transmitted by female worms, and horizontal transmission can occur within the vector Mating will take place only between infected males and female worms **Tetracycline reduces the worm fertility and inhibits the growth of the worm. LPS are responsible for the inflammatory response Bacterial catalase MAY be involved in resistance to oxidative stress |
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How does tetracycline protect against Filariasis?
|
Tetracycline kills Wolbachia, the gram negative bacteria that reside inside Wuchereria Bancrofti
This reduces worm fertility and inhibits growth of the worm |
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Wolbachia in Nematodes
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Wuchereria Bancrofti
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Wuchereria Bancrofti
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Wuchereria Bancrofti - Elephantiasis of Scrotum
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Wuchereria Bancrofti - Elephantiasis of Leg
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Wuchereria Bancrofti - Microfilaire - larva before stage L1
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What is the "worm of the blind"?
|
Onchocerca Volvulus - causes human onchocerciasis
Large worms: Males - 19-42 cm x 0.2 mm Females: 50-60 cm x 0.4 mm |
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What is the epidemiology of O. volvulus?
|
Onchocerca Volvulus
More then 30 million people infected in Africa In some small communities in Africa and Central America, most of the people of middle age and over are blind |
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What is the life cycle of O. volvulus?
|
Humans are infected by the BLACK FLY, when infective juveniles are injected into the human during feeding.
The infective juveniles mature into adults. The adult worms occur in "nodules" just under the skin of the human host. Female worms produce microfilariae whicha re found in the subcutaneous tissues Microfilariae are ingested by a black fly when it feeds |
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What is river blindness?
|
Onchocerciasis, caused by Onchocerca Volvulus
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What is the vector of Onchocerca Volvulus?
|
The Black Fly
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What disease is the Black Fly the vector for?
|
Onchocerca Volvulus - Onchocerciasis (river blindness)
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What are the symptoms for onchocerciasis?
|
Formation of nodules: nodules consist mainly of collagen fibers surrounding one of several adult worms.
Dermatitis due to the presence of microfilariae in the skin - allergic responses or toxic effects after the death of the juveniles (9 months to 2 years) Lesions of the eye ~> invasion of the cornea by microfilariae (10-15 years) |
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How is the diagnosis of Onchocerca Volvulus made?
|
History
Symptoms Microfilaria in nodules |
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What is the management of O. volvulus?
|
Onchocerca Volvulus:
Surgery to remove nodules Ivermectin ~> Microfilaricide ~Acts as inhibitor of GABA mediated conduction in the peripheral nervous system Control of black flies |
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What drug is a Microfilaricide and how does it work?
|
Ivermectin - acts as an inhibitors of gamma-aminobutyric acid (GABA) mediated conduction in the peripheral nervous system
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What is the new approach to treatment of onchocerciasis?
|
Targeting Wolbachia, the gram negative bacteria that lives within Onchocerca Volvulus.
Doxycycline therapy have shown great promise Doxycycline interrupts microfilarial embryogenesis, dramatically decreasing or eliminating microfliaria for at least 18 months after treatment. The drug has modest activity against adult worms, reducing numbers by approximately 50-60% |
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Onchocerca Volvulus
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Onchocerca Volvulus
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Onchocerca Volvulus - Microfilariae
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Onchocerca Volvulus - Progressive Keratitis
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Onchocerca Volvulus - Skin Nodules
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Onchocerca Volvulus
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What is the Eye worm, and what is it's distribution?
|
Loa Loa
Located in West Africa |
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What is the life cycle of Loa Loa?
|
3rd stage juvenile (J3) enters humans when bitten by Deerfly.
J3 ~> J4 ~> Adult in subcutaneous tissues of human Microfilaria (J1) migrate to blood (sheathed) Deerfly bites human, and picks up Microfilaria (J1) in mouthparts J1 penetrates gut wall of Deerfly, migrates to fat body and develops J1 ~> J2 ~> J3 J3 migrates to mouth-parts of Deerfly, where it can infect human again |
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What is the vector of Loa Loa?
|
The Deer fly (Chrysops)
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|
What oragnism is the Deer fly the vector for?
|
Loa Loa
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What are the characteristics of Loa Loa?
|
White worm with smooth cuticle covered with irregular, small bosses, except at the head and tail.
Males are 20-34 mm x 350-430 um Females are 20-70 mm x 425 mm They have extreme longevity, 10-15 years |
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What are the symptoms associated with Loa Loa infection?
|
Adults have a tendency to wander through the subcutaneous connective tissue, creating a Calabar swelling
Adults also migrate through the conjunctiva and cornea |
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What is a Calabar swelling?
|
Red itching swellings beneath the skin caused by Loa Loa present in the subcutaneous connective tissue
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How is the diagnosis of Loa Loa disease made?
|
Travel in endemic region
Worm under the skin or in the eye Presence of microfilaire in the blood Serology |
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What is the management of Loa Loa disease?
|
Surgical removal of the swellings
Chemotherapy: Diethyl Carbamazine - Induces a rapid destruction of the microfilariae ~> allergy Ivermectine Control of Deer flies |
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Loa Loa - Adult Worm
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Loa Loa - Calabar Swellings
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Loa Loa - Eye
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Loa Loa - Microfilariae
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What is the Whip Worm?
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Trichuris trichiura
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