Parasitology 1 Flashcards
Parasite lifestyle factors
Host Establish productive infection Evade host mechs Maintain host viablity and potential spread Successful transmission Not all stages are infective for humans
Productive infection establishment
Needs to get to right tissue
Non-productive infection can cause serious pathology
May be within host or move to another host
How do parasites circumvent various host physical response
Cross skin via vectors and direct penetration
Adhere to GI tract to prevent peristalsis
Sequester to venous/arterial circulation to avoid blood flow
Parasite and immune interactio
2 way street…parasite adapts based on immune response
Parasitic dzs nomrally
Long term chronic
Parasitic dz not always evident…when does it become evident
Change in host status or reactivation due to changes in pathogen
Acute dz outcomes
Pathogen or host induced pathology leads to resolution
Sub clinical outcomes
Immune response leads to potential pathology leads to sterile resolution
Chronic infection…change in immune status leads to symptomatic dz
Actue dz with mild and non-specific dz outcomes
Immune response leads to chronic infection…change in immune status and symptoms
Protozoa
Single celled eukaryotes
Metazoa
Made up of helminths (worms), arthropods (everything else but snails) and molluscs (snails)
Main function of arthropods
Act as vectors and reservoirs for dz
Amoebae
Flagellates
Sporozoa
Ciliates
Crawling motion on a substrate
Use of one of more whip like flagella (includes Kinetoplastids)
Gliding motility
Hair like cilia
Helminth classifications
Nematoda (roundworms)
Cestoda (tapeworms)
Trematoda (tissue and blood flukes)
All endoparasites
Host
Animal where a parasite can establish an infection
Definitive vs intermediate host
Def - adult phase (metazoa) or sexual reproductive phase (proto)
Int - Larval (metazoa) or asexual (protozoa)…obligatory for completion of life cycle
Accidental host
Host that is a dead end for a given parasite…still leads to pathology and dz
Transmission to def host allows
Sexual recombination and diversity
Transmission to IM host allows
Higher levels of parasite in the population
Environmental cyts
Mechanism to surive in envrionment in absence of a host
Dormant state within host
Permits transmission…often a cyst
How are parasites transferred from vertebrae to vertebra
Carniverous
Close contact with animals
Infected waste
Sexual activity or handling of tissues
Life cycle stages reflect
Adaptations to environments
Helminth development
Egg to larval to mature to mating back to egg
Incubation period
Time from acquisition to appearance of symptoms - hours to years
Prepatent period
Time from acquisition to detection - days to years
Can be shorter than incubation…often detect cyst form in feces
Patent period
Time in course of parasitic dz during which parasitic organisms can be demonstrated in the body…don’t need symptoms
Most parasitic dz have
Acute and chronic infection
Most common parasitic dz
Intestinal roundworms
Amoebae protozoa
Entamoeba histolyyica
Acanthamoeba
Amoebae/giardia/trichomonas common themes
Evolutionarily among earliest Facultative anaerobes using carb metab Lack mitochondria EC parasite adhere to epithelium (don't invade) Cause contact dependent cytotoxicity Divide like bacteria (binary fission) Killed by metronidazole
Cyst forms of protozoa
Designed for transmission
Non-replicative
Survive in environment
Typically infectious form
Trophic forms of protozoa
Actively replicating, active growhti nthe host, not involved in transmission
ALL protozoa have trophic, not all have environmental cyst
Entamoeba histolytica life cycle
Infection with cysts
Cyst wall disrupted in GI tract and release 4 nuclei amoeba
Trophozoites form after division
Trophozoites divide in intestine and differentiate back into cysts
Cysts deposited in feces
EH trophozoites can move
To portal vein where they can establish liver infection (extraintestinal)
Also can get to lungs, diaphragm, and brain
Intestinal amebiasis characteristics
Bloody and mucoid diarrhea
Blood in the stool with lack of leukocytes
Look for cysts or trophozoites
Trophozoites may be laden with erythrocytes
Acute symptoms of intestinal amebiasis
Ab pain, bloody mucoid diarrhea, flatulence and ab tenderness
May last 2-21 days
Chronic symptoms of intestinal amebiasis
Occassional bloody diarrhea, weight loss, fatigue
Most people with intestinal amebiasis are
Asymptomatic and shed cysts
Extraintestinal symptoms of amebiasis via EH
Pain in upper right quadrant..tender and enlarged liver with abscess, fever, weight loss
EH effect on liver
Amebic hepatitis…lysis and digestion of hepatocytes
Other sites of EH
Lungs, skin, brain…cysts never outside of intestine
GI tract Entamoeba species
E dispar…oftne confused with EH
DIagnosis of EH
Trophozoites with RBCs in the stool or 4 nucleus containing cysts in the stool
Tenderness in upperright quadrant (use Xray and CAT scan to confimr)
Trophozoites in sputum (lung)
CAT scan/MRI for brain
2 other pathogenic amoebae besides EH
Acanthamoeda castellani
Naegleria fowleri
Free living envrionemtal organisms
Cause severe dz in both healthy and immunocompromised individuals
Acquired swimming in warm lakes
Acanthamoeba castellani eye infection
Conjunctivits, keratitis, and uveitis…contact lens wearers
Diagnose by culturing
Keep contacts clean and avoid swimming in wamr lakes
Acanthamoeba castellani CNS involvement
Invades CNS through olfactory bulb
Causes GAE - seizures, brain disturbs, headaches, death
Cannot be detected in the CSF
Tx of GAE and ocular infection by acanthamoeba
Ketoconazole and surgical excision
Topical azole and cessation of contact lens use
Naegleria Fowleri…including tx and diagnosis
Infects healthy young people (often water sports)
Causes PAME with trophozoites but NO cysts
Death in days (1-3 day incubation)
Can see them in CSF
Amphtericin B to treat
Try to diagnosie with culture
important flagellate to remember
Giardia lamblia
Giardia lamblia life cycle
Flagellated diplomonades with 2 nuclei (look like eyes)
ingest cysts, replicate by binary fission and attach to intest epithelium…upper and small intestine are preferred
Cysts have 4 nuclei
Trophozoites have 2
Beaver fever symptoms
Severe cramps
Non-bloody foul smelling diarrhea with greasy stool due to malabsorption of fat
Asymptomatic will shed cysts for years
Incubation = 3-21 days
Giardia cysts
Resitant to chlorination but not to filtration
Infects many different animals, not just humans
Giardiasis is most prevlanet
Cause of non-bacteiral diarrhea in the US
Risk factors for giardiasis
Unfiltered or unboiled water while hiking (Beaver fever)
Fecal oral
Immune suppresssion
Patholgy of giardia
Attach to intestinal epithelium and efface the villi
Sporozoa we need to know
Plasmodium (malaria)
Toxoplasma gondii
Anopheles mosquito
Used to spread malaria
Only females will spread
Obtaining bloodmeal is essential for eggs
Lay 4-5 clutches per lifetime
Where plasmodia undergo completion of their sexual cyce
Malaria life cycle
Passed to humans…goes to liver as asymptomatic…invades erythrocytes
Completes cycle in mosquito
Plasmodium falciparum
Majority of malrial deaths
6-12 PP period
May not have defined fever periodicity
PLasmodium vivax
Most common cause
Benign tertian malaria
10-17 PPP
Plasmodium ovale
Similar to vivax
14 PPP
Plasmodium malariae
Mildest dz but longest
28-35 PPP
Time of infection of malaria
Bite to when the erythrocytic cycle commences and symptoms are present…also defines how long it takes to detect
Symptoms of malaria
During erythrocytic stage…high dever with defined periodicity
Tertian - day 1 and 3 (vivax)
Quartan - fever on day 4 (seen in plasmodium malarium)
Cerebral malaria
Infected erythrocytes have knobs that make them sticky to linings and RBCs…this causes blockages which leads to multiple strokes
Renal and pregnancy complications can result from P falciparum
AIDS associated opportunistic
Toxoplasmosis
Opportunistic pathogens
Don’t normally cuase symptoms in healthy, but will in immunocomporomised
Life cycle of toxoplasmosis gondii
Cat is the definitive host…bradyzoite becomes oocyst…oocyst leaves in the feces and goes to another anuimal…shifts between bradyzoite (chronic) and tachyzoite (actue)…bradyzoite can be transmitted to humans via undercooked meats
Then can transfer tachyzoite to child
Clinical spectrum of toxo
Congenital
Cerebral toxoplasmosis (from AIDS)
ocular
Most severe toxo complicaton
Toxoplasmic encephalitis…tissue cysts form in brain and muscle
Toxoplamsosis encephalitis
Cerebral abscess leads to multifacotiral neurological symtpoms…lethal if untreated
Txs do not target dormant so you need lifelong tx
COngintal toxo
if mother has no ABs, then still at risk but no infection at time
If IgG, then no risk
If IgM, then potential risk to fetus
Conginetal toxo exposures and when symptoms occur
If 3rd trimester, generally no effect
Can occur in under 26 weeks
Mild dz to spontaneous abortion
Chorioretinitis is typically the first to show…could include failure to thrive, and a bunch of other things
Most (75%) are subclinical
Toxoplasmic hydrocephaly symtpoms
Hydrocephalus
Retinochorditis
intracerebral calcifcation
Psycho/motor retardation
Ocular toxoplasmosis
Consequence of congintally acquired
Could occur in 10-20 years after birth
Untreated could lead to blindness
Cryptosporidium
Diarrheal dz in immunocompromised patients
Does NOT penetrate into cells
Sexual cycle occurs in GI tract and not restircted to single host species
Life cycle of cryptosporidum
Oocyst ingested contained 4 sporozoites…oocysts attach…8 new merozoites form from schizogony…differnetiate into male and female gametocytes that then begin process of oocyst formation
Symptoms of crypto
Ab pain, dirrhea for 3-10 days
Often mistaken for food poisoning
Life-threatening in AIDS patients - persistant dirrhea, malabsorption with severe weight loss
Risk factors for crypto
Both animal and human feces
Contam water sources (can be filtered)
Conditions of crowding
Contact with animal waste
Diagnosis and tx of crypto
Oocysts in the feces and PCR approaches
No effective tx…just rehydrate and control
