-
What are the four vertically transmitted parasites?
- Toxoplasmosa spp.
- Plasmodium spp.
- Trypanosoma spp.
- Trichomonas vaginalis
-
Triatoma (reduviid)
vector for American Trypanosomiasis (Chagas disease)
-
- Trypanosoma cruzi
- (Trypomastigote phase)
- found in bloodstream
-
What is another name for triatomas?
vector for American Trypanosomiasis (Chagas disease)
"kissing bugs"
-
How is Trypanosoma cruzi transmitted?
via feces of triatomas
-
What are the reservoir hosts of Trypanosoma cruzi?
- armadillo
- agouti
- rats
- opossum
- dogs/cats
-
What is the growth cycle of Triatomas?
- hemimetabolous growth
- egg --> nymph --> bigger nymph --> adult
-
- Typanosoma cruzi amastigote stage
- after invasion of muscle/nerve tissue
- destroys tissue during binary fission
-
What are the predilection sites for Trypanosoma cruzi?
- muscle/nerves
- specifically:
- myocardial tissue
- myenteric plexus (peristalsis)
-
How is Trypanosoma cruzi diagnosed?
- in acute stage
- Direct:
- blood smear (thin/thick)
- xenodiagnosis (use triatoma for PCR)
- serology Ag
- DNA probes
-
- Trypanosoma rangeli
- apathogenic
-
- changoma (Romana's sign)
- first sign of Trypanosoma cruzi
-
What is the acute clinical presentation of Trypanosoma cruzi?
- fever
- anemia
- edema
- lymphadenopathy
- hepatosplenomegaly
- EKG abnormalities
- CNS involvement
-
What can occur after the acute phase of Trypanosoma cruzi?
- Indeterminate phase (asymptomatic)
- Chronic phase (30%)
-
What are the clinical manifestations of chronic Trypanosoma cruzi?
- fever
- loss of myenteric plexus:
- constipation
- abdominal distention
- megacolon/megaesophagus
- loss of myocardium:
- EKG abnormalities
- Cardiomegaly
- apical aneurysm
-
How is Trypanosoma cruzi transmitted?
- Triatoma bites
- blood transfusion
- congenital transmission
- lab transmission
- organ transplant
-
Where to Triatomas live?
- South/Central American rainforests
- Trinidad
- *houses built in rainforests
-
How is Trypanosoma cruzi treated?
- Benzimadazole
- Nifurtimox
- - treatment in acute phase
- - Tryptomastigotes only
-
What are the two types of African Trypanosomiasis?
- Trypanosoma brucei rhodensiense
- (Rhodesian sleeping sickness)
- Trypanosoma brucei gambiense
- (West African/Gambian sleeping sickness)
-
- Tsetse fly
- - "meat cleaver" on wing
- - holometabolous growth (egg --> larva --> adult)
- vector for African trypanosomiasis (sleeping sickness)
-
What is the reservoir for T.b. rhodesiense (Rhodesian sleeping sickness)?
- wild animals (antelope/bushbuck)
- does not cause clinical symptoms
causes disease in domestic animals
-
What is the reservoir for T.b. gambiense (West African/Gambian sleeping sickness)?
- Pigs
- (humans are main reservoir)
-
- trypanosomal chancreerythematous tsetse bite
- clinical symptom of African trypanosomiasis
-
- Winterbottom's sign
- enlarged cervical lymph nodes
- first clinical sign of African trypanosomiasis
-
- Trypanosoma brucei
- rhodesiense/gambiense
ONLY as trypomastigotes
-
How is African trypanosomiasis diagnosed?
- Direct:
- T.b. rhodensiense/gambiense
- in blood smear/buffy coat
- gland juice aspiration
- CSF
- PCR
- Indirect:
- IgM ELISA (not useful)
-
What are the clinical manifestations of African trypanosomiasis?
- T.b. rhodensiense - acute (weeks)
- T.b. gambiense - chronic (months)
- fever
- anemia
- wasting
-
What is the treatment for African trypanosomiasis?
- I.V. Suramin
- I.V. Eflornithine (expensive!)
- both do not cross BBB
-
What is the treatment for African trypanosomiasis with CNS involvement?
- Suramin
- Eflornithine
- Melarsoprol (crosses BBB)
-
How is African trypanosomiasis controlled?
- biconical traps for tsetse flies
- insecticide
-
What are the different types of Leishmania?
- Kala-azar (black fever)
- Old world cutaneous
- New world mucocutaneous
-
What are the parasites that cause Kala-azar?
- type of Leishmaniasis
- Leishmania donovani
-
What are the parasites that cause old world cutaneous Leishmaniasis?
- Leishmania tropica
- L. major
- L. aethiopica
-
What are the parasites that cause new world mucocutaneous Leishmaniasis?
- aka "Espundia"/"Uta"
- Leishmania braziliensis
-
What are the predilection sites for Leishmania spp?
- Vertebrate host:
- WBC (amastigotes)
- --> migrate to skin macrophages/inner organs (4-6 days)
- Vector:
- Saliva (promastigote)
-
- Leishmania spp. in WBC
- --> lysis after 48 hours
- --> migrate to skin (cutaneous)
- --> 4-6 days - migrate to organs (visceral)
-
Leishmania promastigotes in saliva of sand flies
-
How is L. donovani (Kala-azar) diagnosed?
- spleen/bone marrow aspirate
- to visualize amastigotes
- rK39 dipstick
-
What are the clinical symptoms of Kala-azar (L. donovani)?
- early:
- double daily fever spikes
- anemia/leukopenia
- diarrhea
- joint pain
- late: hepatosplenomegaly
-
- Fever spikes of Kala-azar
- (L. donovani)
- visceral leishmaniasis
-
What is the treatment for L. donovani (Kala-azar)?
- Amphoteracin B
- --> highly toxic and expensive
- Pentostam (antimonial compound)
- --> cheaper/not well tolerated
- --> developed by One World Health via Bill & Melinda Gates
- Paramomycin
- Miltefosine (oral)
-
Where are sandflies found?
- vector for L. donovani
- Ethiopia, South Sudan, Kenya
- near termite hills
-
What are the clinical symptoms of Leishmania major?
- old world cutaneous Leishmaniasis
- small red papule
- ulcerates (2 weeks)
- serous exudate
-
What are the clinical symptoms of Leishmania tropica?
- Old world cutaneous Leishmaniasis
- small red papule
- ulcerates (2-4 months)
- dry ulcer
-
- Leishmania major
- ulceration in 2 weeks
- with serous exudate
-
- Leishmania tropica
- ulceration in 2-4 months
- dry exudate
- immune response
-
What is another name for L. tropica exudates?
oriental sore
-
How are L. tropica and L. major diagnosed?
- fluid aspiration from ulcer
- look for amastigotes
-
What is another name for Leishmania braziliensis?
Espundia or Uta
-
- Lesions from L. braziliensis
- oral or nasal appear in 3-20 years
-
What are the clinical signs of L. braziliensis?
- new world mucocutaneous
- small cutaneous papule
- ulcerates in a few months
- leaves asymptomatic scar
-
What are the differential diagnoses for L. braziliensis?
- fungi
- syphillis
- yaws
- leprosy
- malignancy
-
What are the treatments for L. tropica, L. major, L. aethiopica, and L. braziliensis?
- Amphoteracin B
- --> toxic/expensive
- Pentostam (antimonial compound)
- --> cheaper/not well tolerated
- --> One World Health (Gates foundation)
- Paramomycin
- Miltefosine (oral)
-
What are the reservoir hosts of Leishmaniasis?
- sloths, rodents, dogs
- found in rainforests
-
- Trichomoniasis
- Trichomonas vaginalis
-
How is Trichomonas vaginalis transmitted?
- sexual transmission
- mother --> infant
-
What are the clinical symptoms of Trichomonas vaginalis?
- vaginitis
- burning
- thick yellow discharge
- vulvular/vaginal erythema
- males asymptomatic
-
How is Trichomonas vaginalis diagnosed?
- Direct:
- trophozoites in urine or vaginal discharge
-
How is Trichomonas vaginalis treated?
Metronidazole (Flagyl)
-
- Giardia lambia
- Giardiasis
- trophozoite form
- found in diarrhea
- not infective
-
- Giardia lambia
- Giardiasis
- cyst form
- found in normal stool
- infective
-
What is the prevalence of Giardia lambia?
- "traveller's diarrhea"
- 2-7% USA, Canada, Europe, Australia
- 40% developing countries
- common in day-care centers
-
What are the animal reservoirs for Giardia lambia?
- beavers
- dogs
- animal form doesn't last as long
-
When should G. lambia be suspected?
- chronic (intermittent) diarrhea
- unexplained weight loss
- unresponding malnutrition
- malabsorption
-
How is G. lambia diagnosed?
- Direct: stool microscopy
- --> low specificity/sensitivity (cysts not always present)
- Indirect: ELISA
- Immunofluorescent slide
- --> expensive
- --> high sensitivity/specificity
- Therapeutic Trial
- = treat it!
-
What are the symptoms of G. lambia?
- pale loose stools 3-8x daily
- flatulence
- abdominal distention
- abdominal pain
- weight loss
- "sulphorous belching"
- +/- malabsorption syndrome
-
How is G. lambia treated?
- Metronidazole (Flagyl)
- Tinidazole (Tindamax)
-
- Cryptosporidium parvum
- in GI tract (enterocytes)
-
How is cryptosporidium transmitted?
- water-borne epidemic
- 1-3% diarrheas in developed countries
- 17% diarrheas in developing countries
-
What are the animal reservoirs of cryptosporidium?
- humans
- bovine
- dog-like genotypes
- mostly in young animals
-
How does autoinfection occur with cryptosporidium?
- thin walled oocysts reinvade gut
- oocysts excreted
- --> fecal-oral contamination
anti-diarrheal drugs
-
How is cryptosporidium diagnosed?
- Oocysts in stool (modified Ziehl-Neelsen stain)
- ELISA (Ag test)
- Immunofluorescent test (IFAT)
- --> most sensitive
-
What are the clinical symptoms of cryptosporidium?
- 1-2 weeks after exposure
- --> explosive diarrhea 2-10x daily
- --> fever, abdominal pain, anorexia, vomiting
- 1 day - several weeks
-
What are the clinical symptoms of cryptosporidium for immunodeficient individuals?
- large volume diarrhea
- --> hypovolemic shock
- weight loss
- malabsorption
- villous atrophy
-
How is cryptosporidium parvum treated?
it's not
no anti-diarrheal drugs
-
- Amoebiasis
- Entamoeba histolytica
-
What are the two types of Amoebiasis (Entamoeba histolytica)?
- Intestinal amoebiasis =
- amoebic dysentary
- Liver amoebiasis =
- Amoebic liver abscess (ALA)
-
What is the prevalence of Amoebiasis?
- one of most prevalent
- affects 10% world population
- mostly in tropics
-
How is Amoebiasis transmitted?
- Fecal-oral ingestion
- (fluid, fingers, flies, fields)
- not zoonotic
-
How is intestinal amoebiasis diagnosed?
- Direct:
- cysts in stool
- trophozoites in RBC (blood smear)
- ELISA (highly sensitive/specific)
-
- Entamoeba histolytica cysts
- found in stool samples
-
What are the clinical manifestations of intestinal amoebiasis?
- 95% asymptomatic
- diarrhea (inconsistant; <12x daily)
- flatulence
- abdominal pain
- no fever
- blood/mucus in stool
- tear drop ulcers in gut
-
What are the clinical manifestations of amoebic abscesses?
- amoebic abscesses in:
- liver, brain, skin, lungs, orbit, spleen, genitals
- fever
- liver pain/tenderness
- hepatomegaly
-
- liver abscess
- 2* to Entamoeba histolytica
- detect via ultrasound
-
How is amoebiasis diagnosed?
- Direct:
- abscess aspiration under US
- trophozoites
- Indirect:
- imaging with serological confirmation
- -ultrasound (liver)
- -X-ray/CT/MRI (brain/lung)
-
How is intestinal amoebiasis treated?
- metronidazole (Flagyl)
- paromomycin (Humatin)
-
How are amoebic liver abscesses treated?
chemotherapy with metronidazole (Flagyl)
drainage of abscess via ultrasound
-
How is Entamoeba histolytica controlled?
- hygiene
- boiling/filter water
- no "night soil" fertilization
-
What is the life cycle of Toxoplasmosa gondii?
- cat ingests bradyzoites (meat) or tachyzoites (raw milk)
- --> cat sheds unsporulated oocyst
- oocyst sporulates in 1-5 days
- all forms infective
-
What is the prevalence of Toxoplasmoa gondii?
- zoonotic
- >30% world population infected
- 3-20% AIDS patients die of toxoplasmosa associated encephalopathy
-
- Toxoplasma gondii
- oocysts
- sporocysts
- sporozoites
-
- Toxoplasma gondii
- tachyzoites (raw milk)
-
- Toxoplasma gondii
- bradyzoites (meat)
- no inflammation present around cyst
- tachyzoites already present in WBC
-
- Tachyzoites transported via leukocyte
- predilection sites: brain/eye
-
What is the largest risk factor of toxoplasmosis?
eating raw lamb, pork, goat
-
When is a fetus most at risk for contracting toxoplasma gondii?
- Transmission rate:
- increases with time (more placental development)
- % severe infections:
- decreases with time (development of fetal immune system)
-
What are the severe outcomes of fetal toxoplasm gondii?
- chorioretinitis
- hydrocephalus
-
How does hydrocephalus occur with toxoplasma gondii?
- bradyzoites enter periventricular areas
- --> obstruction of 3rd ventricle
treat with ventriculoperitonel shunt
-
How is toxoplasma gondii detected?
- IgG, IgM serology
- IgM present at initial infection
- CT with contrast
- MRI
- tissue biopsy (bradyzoites)
-
When should maternal testing occur for toxoplasma gondii?
- (-) IgG --> test monthly for IgM
- (+) IgG --> r/o recent or active infection
- (+) IgM --> prophylaxis and f/u with infant
-
How is toxoplasma gondii prevented?
Prophylaxis with spiramycin
-
How does Plasmodium spp. enter mosquitos?
gametocytes formed by merozoites in the bloodstream ingested by mosquitos
-
What form of Plasmodium spp. enters humans from mosquitos?
sporozoites in mosquito salivary glands
-
Where do Plasmodium spp. sporozoites go once inside human?
- liver parenchyma
- occurs within 30 minutes
-
What happens to Plasmodium spp. in the liver?
- sporozoites can either:
- 1. asexual reproduction -->
- merozoites within schizont2. formation of hypnozoite (P. vivax/ovale)
-
How long does the liver cycle last for Plasmodium spp.?
-
How is Plasmodium spp. infection passed onto the blood?
- 1. schizont releases merozoites2. merozoites invade erythrocytes
-
What happens in the erythrocytic cycle of Plasmodium spp.?
- in erythrocytes:
- 1. merozoites --> tropnozoites --> schizonts
- 2. erythrocyte lysis
- 3. merozoites released
-
How long does the erythrocytic cycle take for Plasmodium spp.?
36 hours for P. falciparum
-
What happens in the mosquito life cycle of Plasmodium spp.?
- 1. gametocytes liberated --> micro/macrogamete
- 2. micro/macrogamete unite --> zygote
- 3. zygote --> ookinete4. ookinete penetrates gut wall
- 5. ookinete --> oocyst
- 6. oocyst --> oocyte
- sporozoites created within oocyte
-
How long is the mosquito stage of Plasmodium spp.?
5 days
-
How long does it take to get symptoms of Plasmodium spp. after a bite?
- 8 days of hepatic cycle
- 36 hours of erythrocytic cycle
- => 11 days total
-
- Anopheline mosquito
- vector for Plasmodium spp.
- (P. falciparum, P. vivax, P. ovale, P. malariae)
-
- Plasmodium falciparum
- - rings with double chromatin dots
- - marginal forms
- - RBC not enlarged
-
- Plasmodium falciparum
- gametocytes
-
- Plasmodium malariae
- - band shaped
- - RBC not enlarged
-
- Plasmodium ovale
- - "oval" red cell
- - enlarged RBC
-
- Plasmodium vivax
- - thick (signet) ring
- - enlarged RBC
-
hypnozoite in liver
- dormant form of Plasmodium vivax/ovaleallows for reoccurrence
-
How does the anopheline mosquito reproduce?
- gonotrophic cycle
- egg --> larvae --> adult
- eggs laid in standing water
-
Where is Plasmodium falciparum found?
-
Where is Plasmodium vivax found?
- Central America
- Southern Asia
-
Where is Plasmodium ovale found?
- West Africa
- **instead of Plasmodium vivax
- --> P. vivax merozoites cannot infect 2* to "duffy" blood group
-
Where is Plasmodium malariae found?
widespread
-
What are the clinical signs of Plasmodium spp. infection?
-
How does the fever cycle relate to the life cycle of Plasmodium spp.?
- 1. release of merozoites --> decreased body temperature
- 2. immune response --> fever spike
- 3. immune response maintenance --> sweating phase
-
Why does the body temperature decrease when merozoites of Plasmodium spp. are released?
- Immune system shunts blood to core (protection)
- skin dry, pale, cold
- pulse rapid, low volume
-
- P. falciparum fever chart
- persistant fever
- fever decreases every 2 days
-
- P. malariae fever chart
- slight peaks every 24 hours
- large peak at 72 hours
-
- P. vivax/ovale fever chart
- fever peaks every 2 days
-
- microcirculatory arrest
- 2* to P. falciparum infection
- hemolysis --> dead tissue aggregation
-
What organs are affected by Plasmodium spp.?
- kidneys --> renal failure
- liver --> jaundice/fever
- lungs --> pulmonary edema
- stomach/intestines --> vomiting/diarrhea
- brain --> delirium, stupor, disorientation, coma, convulsions
-
When is cerebral malaria suspected?
Patient suspected of malaria shows reduced consciousness
-
How does cerebral malaria manifest?
- coma (eyes open; unseeing)
- convulsions
- abnormal posturing
- dysconjugate gaze
- retinal hemorrhages
-
- Cerebral malaria
- schizont adhered to brain endothelium
-
- Decerebrate rigidity
- 2* to cerebral malaria
- --> rigidity of extensors
-
- Decorticate rigidity
- 2* to cerebral malaria
- --> rigidity of flexors
-
What is the fatality of cerebral malaria?
- 20% fatal
- 10% of children with lingering neuropsychological deficits
-
What are the risks of malaria with pregnant women?
- maternal mortality
- abortion
- stillbirth
- premature delivery
- low birthweight
- vertical transmission
-
What are the direct effect of malaria on pregnant women?
- depressed immunity
- parasitization of placenta --> movement hindered
- premature delivery
-
What is the treatment for P. falciparum?
- chemotherapy ASAP!
- **resistance to chloroquine
-
What is the function of quinine (Quinadine)?
- destroys blood stages of Plasmodium spp.
- - no resistance
- - reserve drug
-
How is Plasmodium malariae treated?
- Chloroquine
- destroys all blood stages
- "magic bullet"
-
How are Plasmodium ovale/vivax treated?
- Chloroquine (blood stages)
- Primaquine (hypnozoites)
- --> prevents relapse/reoccurrence
-
What is the treatment for Plasmodium falciparum?
- Quinine, Quinadine
- Artemether/lumefantrine (coartem)
- **ACT - Artemisinin-based Combination Therapy
-
How is malaria treated prophylactically?
- Mefloquine (Lariam)
- Doxycycline
- Chloroquine (Aralen)
- Atovaquone/proguanil (Malarone)**P. falciparum resistant to chloroquine
-
What are the side effects of malaria prophylaxes?
- Mefloquine - neuropsychiatric problems
- Chloroquine - itchy skin
- Pauladrine - mouth ulcers
-
What are the differences between stable and unstable malaria?
- unstable:
- seasonal transmission
- epidemics
- low immunity
-
How does the sickle cell AS phenotype protect against malaria?
- RBC sequestered in RE system
- low pH area --> hinders parasite growth
- fast splenic clearance
-
How was malaria eliminated in Grenada?
- swamp, drain, fish filling
- DDT spraying
-
What are autocthonous cases of malaria and why are they a problem?
- imported malaria (especially from Jamaica)
- merozoites must be present in blood prior to screening
-
How is malaria diagnosed?
- clinical:
- fever
- anemia
- hepatosplenomegaly
- direct:
- PCR to detect DNA
- Rapid tests: parasite antigen
- Parasites in blood smear
-
When do anopheline mosquitos bite?
- at night
- (put up nets with pesticides as prevention)
-
For trematodes, what form infects snails?
miracidia
-
For trematodes, what form infects crabs/fish/fluke?
- cercaria
- fluke also infected by metacercaria
-
- Schistosoma haematobium
- terminal spine
- not zoonotic - only infects bulinus snails
- found mostly Africa and Middle East
leads to urinary syndromes
-
- Bulinus snail
- host of Schistosoma haematobium
-
- Schistosoma masoniegg has lateral spine
- leads to liver pathologies
- infects biomphalaria snail
- mostly Africa and South America
-
How widespread is Schistosoma masoni?
- South America, Caribbean islands, Africa
- reservoirs: humans, rodents, baboons
- causes intestinal schistosomiasis (most important)
-
- biomphalaria snail
- host of Schistosoma masoni
-
- Schistosoma japonicum
- leads to liver pathologies
- infects oncomelania snails
- Southeast Asia
-
Where does reproduction occur for the schistosomes?
- in the liver
- --> migrates to final predilection site
-
How is Schistosoma haematobium diagnosed?
- indirect:
- serology
- gross hematuria
- dipstick
- imaging
-
- Ultrasound of Schistosoma haematobiumcheck for areas of bladder wall thickening/polyps
-
How are Schistosoma mansoni/japonicum diagnosed?
- direct:
- eggs in stool
- rectal biopsy
-
- pipe-stem fibrosis
- Schistosoma masoni/japonicum
- 2* to eggs being swept back into liver
- (normally --> mesenteric veins)
- become calcified
-
- Phnom Pehn-Vientiane
- Schistosoma japonicumcalcification of capillaries
- --> "fishnet" appearance
-
Which of the Schistosomas lead to the highest morbidity/mortality?
Schistosoma japonicum
-
What is the progression of schistosomiasis?
- 0-3 days: swimmer's itch
- (penetration of schistosomulum)
- (migration of schistosomulum)
3-6 weeks: acute schisto ( Katayama Fever)
-
What are the characteristics of acute schisto (Katayama Fever)?
- 2* to egg laying
- acute febrile reaction
- eosinophilia
- lasts 3-8 week
-
- Chronic Schistasomiasis
- --> eggs trapped
- --> inflammation (granulomatous/fibrosis)
-
What are the characteristics of chronic infection by Schistasoma haematobium?
- thickened bladder wall
- polyps (--> cancer)
- ureter obstruction
- hydronephrosis
-
- hydronephrosis
- 2* to chronic Schistasoma haematobium
-
What are the manifestations of chronic Schistasoma masoni/japonicum?
- periovular granuloma
- - hepatosplenic inflammation
- - hepatosplenomegaly
- - liver fibrosis
- - portal hypertension
- 2* to eggs trapped in mesenteric veins/portal vein and branches
-
How are Schistasoma spp. treated?
- Praziquantel
- --> effective for children
existing fibrosis not reversible
-
What factors influence the prevalence of schistasomiasis?
- Schistasoma spp. favor:
- - low altitude
- - rainy area
- - proximity to lake
-
How was Schistasoma japonicum eliminated in Japan?
- water buffalo are intermediate hosts
- --> start using tractors
- China control program:
- treat/vaccinate water buffalo
-
When are schistasoma spp. cercaria shed?
in the midday
-
What are methods for controlling Schistasoma spp.?
- kill parasite (Praziquantel)
- - treat school-age children 2-3x
- kill snails
- prevent contamination (drinking water/latrines)
- protect from infection
funded by Gates Foundation/World Bank
-
Why are children more likely to get Schistasomiasis?
- reinfection for adults lower
- - possible immune response
- children more likely to play in water (behavioral difference)
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