Parasitology 2 Flashcards
Important kinetoplastids and dz caused
Trypanosome brucei (sleeping sickenss) Trypanosoma Cruzi (chagas) Lesihmania (Leishmaniasis)
Kinetoplasmid features
Flagellar pocket
Single mitochondrion with genome in kinetoplasts
Lipid anchored coat proteins
All transmitted by insect vectors
African sleeping sickness, cause and transmission
T brucei ganbiense (west coat)
T brucei rhodesiense east coast)
Tsetse fly
T brucei uses what to help invade
VSG (antigenic variation)
ABs raised against VSG…different VSG gene expressed and avoid ABs…keeps doing this
Stage 1 of T brucei
Infection initiated by bite…forms chancre or Winterbottoms sign…ID prasites in biopsies…gambiense harder to ID
Stage 2 of T brucei
Trypanosomes enter bloodstream and start binary fission…activates immune response to VSG (class swithcing enhances survivial)…Symptoms include high fever and fatigue, facial edema, and macular rash on trunk (rhodiense)
Symptoms of T brucei will
Will follow pattern of elimination
Rhodesiense will manifest 1-3 weeks after
Gambiense takes much longer
Stage 3 and 4 of T brucei
3 - lmyphatic invasion - fever
4 - Involvement of CNS
Gambiense progression takes 9 mos to 3 years
Rhodesiense over 3 months
Chagas dz transmission
Riduviid bug defacates on skin while feeding and scratching rubs it into the skin
Chagas life cycle
Parasites infect macrophages and differentiate from trypomasitgotes into amastigotes by losing flagella…will turn back into trypomastigotes in order to go back to the vector…differentiate into epimastigote back in the ruduviid bug
Chagas dz
Chagoma or Romana’s sign at bite - 5-20 days after
Can lie dormant for many years - affedcts heart, seophagus, and colon
Chagomas occur around the eyes or lips where bugs bite
T cruzi cardiax
Destruction of cardiac tissue…immune response damages and replacves with firbotic tissue…hypertrophic thinning of ventricular wall which can lead to heart attack
Other chagas symptoms
Megaesophagus and megacolon
Chagas encephalitis - death in 1-2 months
Abortion
Chronic chagas resolves spontaneously but asymptomatic may last for decades
Lipochagomas or lipogranulomas in dermis of adipose tissue
Detection of chagas and periods
Can use blood smear, PCR, etc.
Incudbation - 5-20 days (chagoma formation)
Prepatent - 1-2 months
Patent - 20 years
Leishmania dzs and transmission
Cutaneous
Mucocutaneous
Visceral (kala azar)
By snadflies of phlobotomus or lutzomyia
Leishmania life cycle
Amastigotes ingested and differnetiate into promastigotes…bind to sandfly midgut and proliferate…
In mammal, parasite infects macrophages and differentiate into amastigote…L donovani and visceral will perpetuate amastigtoe cycle in reticular-endothelial system and other internal organs…cutaenous will not…
Cutaneous leishmanias organisms, periods, and diagnosis
L tropica and major in Afghan and iraq
L mexicana in new world
Incubation - 2-4 weeks to a year
Prepatent - 1-3 months
Patent - Months
Diagnose with amastigotes in skin biopsies and serodiagnosis
Mucocutaneous leishmanias organism and mech
L brasiliensis
Disfiguring of the face due to metastasis of dermis
Target mucous membranes in oral-naso pharyngeal region
Kala azar organisms and periods
Old - L donovani and infantum
New - chagasi
Incubation - 10days to a year
Prepatent - 1-3 weeks
Patent - months to year
Kala azar mech
Able to replicate in internal organs…will cause heptao and splenomegaly
Hyperactive spleen results in removal of RBCs from circulation causing anemia, hypoalbuminea and hyperglobulimia…Igs deposited on the kidneys…infection of bone marrow leads to secondary infections
Acute symptoms of kala azar
Fever peaking at 24 hours…lethargic and cachexic
Post kala azar dermal leishmanieas
Resolution of dermal symptoms leaves nodular skin lesions on the face
Detection of kala azar
Tissue from biopsies and bone marrow
Nematoda
Cestoda
Trematoda
Nematoda - roundworms
Cestoda - tape
Trematoda - flukes
Primary worm routes of infection
Ingestion
Skin penetration
Vector mediated
Helminth infection recurring themes
Long term and chronic Widespread Humans can be any kind of host Symptoms at all life cycles Host response often associated with symtpoms
Host resonse to helminths
Low incidence of severe dz Morbity but minimal mortality Long term and chronic Th2 like response IgE response with eosinophilia and mast cell responses
Generalized helminth life cycle
Maturation step results in fertilized egg (embryonation)
Maturation to adult
Male and female adults release eggs (at any stage of embryonation) or live larvae into the environment
Humans infected by
Eggs from enviornment
Cutaneous penetration of larval stages
ingestion of mean of larval stages
Insect vectors
Pathology due to
Direct damage
Migration of worm
Immune response
Orally ingested pinworms and what they cause
Ascaris lymbricoide (ascariasis) "non human" ascaridis (visceral larva migrans)
Nematodes
Nematode sturcutre
Tubular or cylindrical body plan
Ascaris is most common worldwide
Enterobius most common in US
Ascariasis geographic and basic mechanism
South and SE US
Compete with host for nutrients and cause bowel obstructions
Ascariasis life cycle
Eggs shed in feces of animal and embryonate in the soil…eggs infect the human host and cross from intestine to liver to heart and eventually lungs…L3 formed in lungs and coughed up to the trachea to the pharynx and then swallowed…release eggs
Symptoms of ascariasis and periods
Resp symptoms with eosinophilia
Peritonitis
Can occlude bile duct, esophagus, mouth, pancreatic duct and liver
Aggregation can obstruct intestine
incubation - 1 week for lung
3 week for intestines
Most have no symptoms
Live 9-15 months
VLM life cycle and pathology
Ascarid parasites of dogs and cats…cannot complete cycle in humans
Ingest embryonated eggs…migrate into circulation
Attacked by eosinophils and form granulomas
VLM symptoms
Ocular damage to the retina from granuloma…often mistaken for retinoblastoma
Most asymptomatic
CNS involvement as well
Skin penetrating nematodes
Hook worms Animal hookworms (cutaneous larva migrans)
Life cycle of hookworm
Filarform larval stage penetrates and goes to lungs…get to GI by coughign and swallowing…develop into male and female in the GI and anchor using hooks…female sheds eggs that are partially embryonated and pass through gut
Dz of hookworms
Cutaneous symtpoms of rash and itching
Focal hemorrhage and allergic pneumonia if in the lungs
Stool appears black, lots of blood loss, anemia, cechexia and breakdown of ciruclation
Hookworm periods
Incubation - derm - 4h, inteestinal 2 weeks
prepatent - 5-6 weeks (egg)
Patent - 20 years (chronic reinfection)
Cutaneous larva migrans
Humans are not def host and larvae are developmentally arrested…migrate throug skin and triggers serpiginous rash
Treat with albendazoels
Occlusion of lymphatic system by lymphotrophic filial worms results in
Elephantitis
Filarial worms targeting eye
Loa loa
Onchocerca volvulus
Cestodes morphological
Anterior portion - scolex (attachment)
Proglottids - segments that have both female and male organs
Basic cestode life cycle
Ingestion of eggs or cyst
Scolex attachment in gut
Maturation of proglottids
Release of gravid proglottids and eggs into feces
Cestodes we need to know
Taenia solinum (pok tapeworm) cystercircosis Taenia saginata (beef tapeworm)
Cestode eggs and larvae
Eggs released from gravid proglottids and embryonate
Acquire a thicker wall out of which 6 hooks project…this is the infectious oncosphere
Beef and pork tapeworms
Humans are definitive for both
Eggs are passed only in human feces
Taeniasis
Intestinal phase of the dz
Extranintestinal pathology
Cysticercus cellulosa and bovis or intermis
Life cycle of tapeworms
Worms attached shed gravid proglottids and embryonate to form onchosphere…cannot complete lifecyle cysticerus form in muslce…mature in the human gun to adults
Symptoms of tapeworms
Weight loss, malnutrition, ab pain, anal itching
Ectopic larval stages can cause
Brain damage, eye damage, liver damage
Pork will form cysticerus cellulosa
Diagnosis of tapeworm and periods
Intestinal stages - passing proglittids and eggs in stool
Organ involvement of pork tapeworm
Can remove using surgery
Incubation - 8-10 weeks
Prepatent period - 8 weeks
Patent period - 25 years (intestinal)
2 years (cysticercosis)
Trematode organisms
Schistosoma mansoni (intestinal schistosomiasis) Schistosoma heamotobium (urogen schisto) Bilharzaria variglandis (cercarial dermititis (swimmers itch)
Trematode morpho
Leaf or oval shaped
Mating pairs for life
Blind alimentary canal
Locomotion by muscle movement
Many use snails as IM hosts
Life cycle of treamtode
Cercariae burrow into skin or swallowed…migrate to mesenteric veins around colon or peliv veins around bladder…eggs are shed into feces or urine
Intestinal schisto symtpoms
Acute symptoms 14-84 days post infection
Fever, headache myalgia…pain and tenderness in upper right quadrant (hepatomegaly)
S mansoni assoicated with resp
Eosinophilia
Coincide with deposition of eggs
Chronic schisto (intestinal)
Bulk of patho caused by immune response to eggs and granuloma formation…pushes into lumen of the bowel
Intestine and liver are main sites of granuloma
Symptoms chronic schisto (intestinal)
Hypogastirc pain with blood in the stool
Diarrhea alternates with constipation
Liver - fibrosis due to egg burden causes hepatomegaly…triggers anemia and ascites dueto liver damage
Urogen schisto
Hematouria
due to deposition of eggs into bladder mucosa and granuloma formation
Woemn susceptible to female genital schistosomiasis
Ectopic schisto
Pulmonary involvement leads to pulm hypertension and cardiac hypertrophy
CNS involvement
In childhood, can exhibit anemia and growth retardation
Intestinal and urinary schisto periods
Int , urin
Incubation - 1-3 weeks, 4-7 week
Prepatent - 4-7 weeks, 9-10 weeks
Patent - 25 years, 25 weeks
Tx of ectopic schisto
Praziquantel and tetrahydroquinolones
Microbilharzaria variglandis
Swimmers itch
Cercarial dermatitis
Infection is a dead end
Rash and localized edema treated with steroids/antihistamine
