Parasitology 2

Question 1

Amebiasis
Location:
Transmission:
Epidemiology:
Immunity:
Diagnosis:

Answer 1

Location: Lumenal; intestine leads in invasion of tissues
Transmission: ingestive; fecal/oral, Direct; anal sex
Epidemiology: US (endemic) - institutions, anal sex
US (epidemic): ex. faulty water purification
Immunity: Humoral responses in invasive disease - maybe acquired immunity in endemic areas
Diagnosis: cysts in stool, travel history, PCR, aspirate of liver abscesses

Question 2

Amebiasis Pathology

Answer 2

Carriers - chronic for months or years
- Shed millions of cysts/day
Dysentery - Severe bloody diarrhea
- Invade colonic epithelium; submucosal ulcers
Invasive - Rare; not always associated with dysentery - Dissemination throughout body, mostly liver

Question 3

Amebiasis life cycle

Answer 3

Infective acid-resistant cysts ingested, excystation in distal small intestine
Trophozoites attach to the colonic mucin and divide
Resistant cysts form in large intestine and are shed in feces
Trophozoites can penetrate the mucosal layer, leading to invasive disease

Question 4

Giardiasis 
Location:
Reservoir:
Transmission:
Epidemiology:
Immunity:
Diagnosis:

Answer 4

Location: Lumenal; intestine
Reservoir: Wild and domestic animals
Transmission: Ingestive: fecal/oral
Epidemiology: Worldwide distribution (epidemics in day care centers, nurseries and ski resorts)
Immunity: uncertain - humoral responses seen in volunteers and resistance in endemic areas
Diagnosis: Stool examination, presence of cysts - Giardia antigen test (ELISA)

Question 5

Giardia Lamblia lifecycle

Answer 5

Trophozoites excyst in upper small intestine
Adherent trophozoites multiply by binary fission
Encystation in large intestine
Excretion of cysts

Question 6

Giardiasis Pathology

Answer 6

Onset at 2 weeks; asymptomatic to explosive diarrhea
Belching, cramps, nausea
Acute usually cure in 1-4 weeks or chronic malabsorption syndrome

Question 7

Apicomplexan parasites of humans

Answer 7

Crytosporidium hominis and parvum - intestine (AIDS)
Toxoplasma gondii - Blood and Tissues (AIDS)
Plasmodium - Blood (everyone)
Babesia microti - Blood (rare)

Question 8

Apicomplexan parasites: Characteristics

Answer 8

Obligate intracellular parasites
Apical intracellular organelles for host cell invasion
Complex lifecycles alternate between asexual and sexual reproduction
Sexual cycle in the intestinal epithelial of definitive host

Question 9

Cryptosporidiosis
Location:
Reservoir:
Transmission:
Epidemiology:
Diagnosis:

Answer 9

Location: Lumenal; intestine
Reservoir: Wild animals/livestock
Transmission: Fecal/oral
Epidemiology: Common secondary infection associated with AIDS - 1993 Milwaukee outbreak
Diagnosis: Acid fast 2-5mm cysts in stool, red ‘cup and saucer’ shaped - now immunofluorescence

Question 10

Cryptosporidiosis Pathology/Immunology

Answer 10

• 3+ water bowel movements in 24 hr
• Profuse watery diarrhea
• Shedding of oocysts highest in acute phase
• Similar to Giardia; shorter, greater fluid loss
• Immunocompromised: more severe; failure to resolve

Question 11

Toxoplasmosis: immunocompromised and pregnancy
Location:
Definitive Host:
Transmission:
Epidemiology:
Immunity:
Diagnosis:

Answer 11

Location: Tissue/blood
Definitive Host: Cats
Transmission: Ingestive: fecal/oral and undercooked meat - transplacental; congenital infection
Epidemiology: Undercooked meat and cat feces
Immunity: Immunodeficient cannot control primary/reactivated infection
Diagnosis: Serology; indirect immunofluorescence - confusion or seizure in immunocompromised (IgG avidity)

Question 12

Toxoplasmosis Pathology

Answer 12

Initial acute infection; often asymptomatic
Rapid control by cellular mediated immunity
Life long latent infection with sub-clinical reactivation
In utero infection - mild to severe consequences - birth defects

Question 13

Toxoplasma Lifecycle

Answer 13

Asexual cycle in Humans/domestic animals

Sexual cycle in cats (hunters)

Question 14

Babesiosis
Location:
Definitive host:
Intermediate host:
Transmission:
Epidemiology:
Pathology:
Diagnosis:

Answer 14

Location: Only red blood cells
Definitive host: Deer tick
Intermediate host: Mice and small mammals (humans are accidental hosts)
Transmission: Nymph stage of deer tick (assoc. w/ lyme disease)
Epidemiology: Northeast and Upper Mid-West US
Pathology: Usually nothing, but some have hemolytic anemia and nospecific flu-like symptoms
Diagnosis: Microscopy to see Babesia inside red blood cells

Question 15

Babesia Lifecycle

Answer 15

2 Tic bites needed on same intermediate host in order for infection to spread

Question 16

Diagnosis between babesiosis and malaria

Answer 16

In RBCs, Babesia has cross-shaped structure “Maltese cross”

Question 17

Malaria
Location:
Definitive host:
Intermediate host:
Transmission:
Epidemiology:
Immunity:

Answer 17

Location: Hepatocytes then erythrocytes
Definitive host: Mosquito
Intermediate host: Humans (primates usually for P. knowlesi)
Transmission: Vector-borne: female mosquitoes
Epidemiology: 2 billion at risk; most fatalities in children and prima gravida females (1st preg)
Immunity: slow to develop; requires multiple infection - short lived

Question 18

Malaria life cycle

Answer 18

Sporozoites from mosquito salivary glands
Go to liver and enter red blood cells as Merozoites
Reuptake into Mosquito as gametocytes

Question 19

Human Malaria species (Global distribution and Relapse from liver?)

Answer 19

P. falciform - 80-90% in Africa, 40-50% in Western pacific and SE Asia, 4-30% in S Asia, S America
- No relapse from liver
P. Vivax - 70-90% in most of Asia and S America; 50-60% in SE Asia and Western pacific; 1-10% in Africa
- Yes relapse from liver
P. Ovale - 8% in parts of Africa
- Yes
P. Malariae - 2-3% in Africa, sporatdic in Asia and S America
- No relapse in liver, but in blood up to 30 years
P. Knowlesi - Reported from SE Asia: 70% in some areas
- No relapse from liver

Question 20

Malaria pathology

Answer 20

Fever cycle with ‘synchronous’ bursts of merozites
P. vivax and P. ovale - 48hr spike
P malariae: 72 hour spike
P. falciparum: 48hr broad then dips
- Anemia results from erythrocyte destruction
Cerebral malaria extreme result of P.falciparum only
Latent hepatic forms in P. vivax and P. ovale

Question 21

Cerebral Malaria

Answer 21

Cerebral malaria syndrome defined by an unarousable coma, ot attributable to other causes, with any level of P. falciparum parasitemia
1% of P. falciparum infections progress to CM and 10-20% of these cases die
Usually seen in children > 2yrs (immature immune system)

Question 22

Respiratory Distress Syndrome

Answer 22

Can be caused by injury to lung micro-vascular endothelium and alveolar epithelium via proinflammatory mechanisms

Question 23

Anemia

Answer 23

Caused by P. falciparum and P. vivax
Destruction of parasitzed RBC by developing parasites-decreased oxygen transport
Increased rate of removal of uninfected RBC
Immune destruction of RBCs coated with parasite derived molecules
Early in life < 2 years

Question 24

Malaria diagnosis

Answer 24

Microscopic tests - Geimsa stain of thin and thick smears remain standard
P. falciparum: multiple rings per RBC - no trophozoites or schizonts
Non-microscopic tests - PCR or rapid dipstick immunoassay

Question 25

Malaria resurgence

Answer 25

After 5 years, malaria eradication programs ended because of slow progress due to increasing insectiside and anti-malarial resistance leaving hundreds of millions susceptible to disease

Question 26

Malaria: Vector Control

Answer 26

Mosquito must take 2 blood meals to transmit parasite
Barriers - insecticides or insecticide impregnated bednets
Release of sterile mosquitoes
Construction and release of bio-engineered mosquitoes