Download Protozoans

Protozoans
Trichomonas Vaginalis
Basic Characteristics
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Flagellated Protozoan
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Exists mainly in trophozite stage and
can’t survive outside of host
Organism only resides in female lower
genital tract and male urethra. It is
noninvasive so can’t cause systemic
infection.
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E. Histolytica (Amebiasis)
Single nucleus org. with ingested RBCs
Naegleria Fowieri
Acanthomoeba
Giardia
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Frothy discharge (yellow green)
Strawberry cervix
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Pruritis, vaginitis
Eosinophilia
pH>4.5= malodorus
Transferred via fomites
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Think Abscesses (anchovy paste)
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Associated with poor water quality and travel
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Disseminates into brain, liver, etc. and for
abscesses
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Symptoms: acute infection causes dysentery with
abdominal pain, chronic infection causes recurrent
episodes with dysentery & dissemination to liver,
brain, lung.
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Flask Shaped Ulcers on biopsy
Treatment
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Metronidazole
Safe Sex
Treating partner very important since males are
often asymptomatic
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Metronidazole for symptomatic
iodoquinol for asymptomatic
Must use both
Paromomycin is the drug of choice
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amphotecerin B shown to work in vitro
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infects the brain (meningitis)
Patient comes in obtuntded, very sick with eosinophilic
meningitis points to naegleria, toxoplasma, or Cryptococcus
Altered sense of smell early in disease process
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Causes keratitis, contact lenses predispose
Destroys cornea
Think Keratitis when you think acanthamoeba
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Difficult, some topical regimens available
Polyhexamethylene biguanide, and many more
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Campers drinking from mountain stream is classical
presentation
Abdominal distension, diarrhea, flatulence
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Metronidazole
In pregnant women use paromomycin as
replacement (1st trimester)
Motile trophozoites in a wet mount
Life Cycle
a) Starts with a mature cyst that is ingested & travels
to small intestine
b) Traveling into small intestine there is
transformation back into trophozites that multiply &
are excreted in the small intestine
c) Main stages of trophozites are diagnosed either in
stool as mature cysts or as trophozites from
different organs
d) Can have either asymptomatic infections,
intestinal dz or extra intestinal abscesses
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Diving and swimming in warm waters
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An amoeba
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THINK CONTAMINATED CONTACT LENS
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An amoeba
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Most common parasite in US
Animals are a reservoir
Manifests in small intestine, not
dysenteric ds! (unlike E.Coli and Shigella)
Fatty stools THINK of bad smelling,
floating stool (CAMPING)
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Clinical Presentation
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Cryptosporidium
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Trypanosome Brucei
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Think community outbreak with
cryptosporidium
Haploid and diploid stages
(oocystssporozites which differentiate
into merozoites in GI tract)
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Voluminous diarrhea
More severe in immune-compromised
Leads to dehydration
Acid Fast Oocysts (same as Giardia, but more commonly
associated with immune compromised)
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Treat with nitazoxanide (new drug)
Requires a vector (tse-tse fly in Africa)
Genetic variation is a big deal with this
(host-organism fight back and forth with
Ag variation, eventually host loses)
KNOW ABOUT ANTIGENIC VARIATION
WITH THIS BUG
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African Sleeping Sickness
Happens when parasite enters CNS
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Blood stage use pentamidine (has a lot of
toxicities hypoTN, nephrotoxic, etc); can’t
penetrate CNS
CNS stage use melarsoprol (can have reactive
encephalopathy); if you can’t Tx E. African brucei
w/ first dose multiple won’t do anything (W.
African is effected w/ multiple dosing)
Can use eflornithine for W. African T brucei
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Trypanosome Cruzi
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Found primarily in S. America
Think C’s
Cruzi, Chagas, Cardiac, megaColon,
Children
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Chagas disease
Cardiomyopathy, megaesophagus, megacolon
ANS ganglia destruction
Inflammatory response ds.
Swelling around eye is one of the first signs (Romana Sign)
Leishmania donovoni
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Toxoplasmosis
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Transmitted by sand fly
Macrophages take up promastigote
which then differentiate into amastigote,
infection propagated by amastigotes
Rarely manifests in immunocompetent
Most of population is seropositive
Intracelluar replication thus CMI
response
Spread by cat feces and pork
CNS disease in AIDS patients (ring
enhancing lesions)
THINK pregnant woman w/ cats
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3 forms of Leishmaniasis, each caused by a different organism
Visceral is most serious form (internal organs affected)
Cutaneous forms skin ulcers
Mucocutaneous is disfiguring
Think: Congenital defects!
Part of ToRches
Generalized lymphadenopathy, thrombocytopenia is
associated with this infection
Also associated with chorioretinitis (loss of eye sight later life
due to congenital defect earlier in lfe)
Falciparum, vivax, ovale, and malariae are
subtypes
Damage is from immune system
Spread by Mosquito (anopheles)
livershizontmeroziteruptures
invades bloodstreamerythrocytic
shizontruptures
Febrile periods follow cycle of red cell
lysis
Vivax, ovale hang out in liver
Falciprum and malariae don’t hang out in
liver
Duffy blood group antigen is receptor for
vivax
Unique because it infects blood
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Plasmodium (malaria)
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IF someone comes from a third world country with high fever
and respiratory distress think malaria
Falciparum binds to postcapillary endothelial cells and
noninfected RBC’s. Can cause occlusion of blood flow.
Sickle cell patients have protection against malaria
Falciparum gives the worst clinical picture
Malariae has 72 h fever spikes, has rosette shizonts
Falciparum, vivax, and ovale have 48 h fever spikes
Falciparum has crescent shaped gametes and trophozoate
sometimes look like signet cells.
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Stibogluconate Sodium (affx redox sys of bug)
Side effx: pain at injection site, chemical
pancreatitis, BM suppression, muscle and joint
pain
Treat with TMP-SMX or atovaquone for
prophylaxis
Pregnant women should avoid cat litter (only
causes congenital defects if mother infected
while pregnant, being seropositive before being
pregnant doesn’t cause congenital defects)
Avoid cat litter
Quinine derivatives for RBC stage(won’t kill
gametes of falciparum), quinidine is used for lifethreatening falciparum , Primaquine for vivax
and ovale in liver stages (give w/ food to mimze
GI distress; can cause hemolytic anemia in G6PD
def pts)
Falciparum is resistant to chloraquine often
Mefloquine resistance in N. Thailand
Tx p. falciparum w/ Malarone
(atovaquone/proquanil)
Metazoans (nematodes,
flatworms, flukes)
Ascaris lumbricoides
Basic Characteristics
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Large intestinal round worm
Clinical Presentation
Treatment
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Degree of disease related to number of organisms present
Larva move from lungs to small intestines
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Mebendazole inhib tubulin dimer formation;
teratogen, pyrantel pamoate
Asymptomatic with eosinophilia
Symptoms: Purpura, eosinophils in lungs, intestinal problems
Eggs not in stool, they hatch in intestines
Filariform larvae penetrate skin and initiate infection, or can
have autoinfection from larvae in intestines
If immunosuppressed, then preexisting infection can become
apparent
Think about this in G-sepsis, travels back up then down into
GI system from respiratory (re-infection)
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Ivermectin inhib glutamate gated Cl- channels
and GABA gated channels, which are located in
bugs but in CNS in humans (selectivity)
Egg of Acaris lumbricoides
Strongyloides stercoralis
Enterobius vermiculars
Taenia saginata & solium
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Autoinfection
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Hyperinfection in the
immunocompromised (disseminated
infection with abdomen/respiratory
distress and GNR sepsis)
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Pinworm infection
Most common helminth infection in US
THINK perianal itchness
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Perianal irritation
Dx. By finding adults/eggs in perianal region
“Scotch tape test”
No eosinophilia because no tissue invasion.
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Pyrental pamoate binds nicotinic receptors
and causes spastic paralysis
Sanitize bedclothes
Treat entire family
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Cestodes
Scolex=head with sucking part
Proglottids= segment that produce eggs
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Prazinquantel
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Saginata has very little symptoms unless infection is heavy
(beef)
Solium eggs are infectious, cystiercosis can develop (pork)
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Dx. By eggs in stool
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Schistosoma spp.
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Trematode
Blood fluke
S. mansoni (Africa), japonicum (Asia),
haematobium (Africa)
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Life cycle involves snails (intermediate hosts) and mammals
(primary hosts)
Snail control is important for disease control. Infections often
occur after swimming in fresh water.
Get dermatitis due to penetration of infectious forms
S. haematobiumbladder granulomas (also associated with
bladder cancer  squamous cell)
S.mansoni/japonicumperiportal
fibrosis/hepatosplenomegaly
Hypersensitivity to eggs is major cause of pathology
dx. with egg in urine or stool
dx. by egg in stool (classic pics below)
Female sexual parts are inside male
S. mansoni. Remember: shistosoma
mansoni has a subterminal spine
S. haematobium. Remember: shistosoma
haematomium has a terminal spine
S. japonicum.
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Praziquantel  incr permeability to Ca++
(hepatic metab via CYP 450)