Protozoal Infections

Question 1

Malaria

Answer 1

Mosquito-borne, hemolytic, febrile illness.
Plasmodium spp.
Infect and drestroy RBCs, splenomegaly
Transmitted by anophales mosquito
Merozoites- daughters or sporozoites feed on Hb & grow and reproduce in RBCs
Rupture of RBCs caused release of pyrogens
Anemia results due to hemolysis & sequestration of RBCs in enlarging spleen

Question 2

Plasmodium falciparum

Answer 2

Agent of Malignant Malaria- predominant in Africa
Causes the more severe disease–> death
No secondary exoerythrocytic (hepatic) stage, parasytizes RBCs of any age, may be several parasites within a single RBC, alters flow characteristics and adhesive properties of infected RBCs so that they adhere to and endothelial cells and small BV leading to ischemia of tissue

Question 3

Plasmodium malariae

Answer 3

Mild form of Malaria
Least common agent
Broad geographical distribution

Question 4

Plasmodium vivax

Answer 4

Common agent of Malaria infection

Rare in Africa, bc population lacks the proper receptor on their RBCs

Question 5

Babesia

Answer 5

Malaria-like infection
Transmitted by hard-bodied ticks
Invade and destroy RBCs,causing hemoglobinemia, hemoglobinuria and renal failure. 
Self limited
Resistant to most anti-protozoal drugs

Question 6

Toxoplasmodium gondii

Answer 6

Toxoplasmosis
Most infection are asymptomatic unless in immunocompromised or in fetus, which leads to a devastating necrotizing disease
Host: cat, ingests cysts
Acute infection: tachyzoites
Chronic Infection: Bradyzoites
Transmittion: eating undercooked lamb, pork, cat feces

Question 7

Toxoplasma Lymphadenopathy

Answer 7

Occurs in immunocompromised patients

Usually resolves spontaneously in several weeks to months

Question 8

Congenital Toxoplasma Infections

Answer 8

Primarily affect the brain
Infection in the fetus is more destructive than in postnatal infection
Necrotizing meningioencephalitis
Fetal infection often leads to spontaneous abortion

Question 9

Toxoplasma Encephalitis

Answer 9

Immunocompromised hosts
Most cases reflect reactivation of latent infections
Brain is most commonly affected and produces a multifocal necrotizing encephalitis.
Fatal if not treated

Question 10

Entamoeba histolytica

Answer 10

Amebiasis: Involves the colon and occasionally the liver
**Humans are the only known reservoir
Transmitted by ingestion of materials contaminated with human feces
There are 3 distinct stages

Question 11

Amebiasis Amebic Trophozoite Stage

Answer 11

Found in stools of patients with acute symptoms
Trophozoites sometimes contain phagocytosed RBCs
Develop into cysts- non-motile, form glycogen masses and chromatoidal bodies

Question 12

Amebiasis Amebic Cystc

Answer 12

Infecting stage and are found only in stools, they do not invade tissue.
These contaminate water, food
Upon ingestion cysts traverse the GI tract and excyst in the lower illeum.

Question 13

Intestinal Amebiasis

Answer 13

Ulcerating disease of the colon
Lesions begin as small foci of necrosis that progress to ulcers
Trophozoites are found in these lesions
Ameboma- infrequent complication, invasion of the intestinal wall, causing intestinal thickening of the bowel wall

Question 14

Amebic Liver abscess

Answer 14

Major complication of Intestinal amebiasis
Trophozoites that have invaded the submucosal veins of the colon enter the portal circulation and reach the liver
Organisms kill hepatocytes, producing slowly expanding necrotic cavity
Severe RUQ pain

Question 15

Cryptosporidiosis

Answer 15

Enteric infection that causes diarrhea in persons w/ compromised immunity. Oocytes survive passage through stomach & release forms that attach to microvillous surface of small bowel.
**Remain extracellular
Profuse watery diarrhea- constant in immunocompromised patients, resolves in immunocompetent patients

Question 16

Giardia lamblia

Answer 16

Infection of the small intestine
Flagellated
Children are more susceptible/ Acquired by ingesting the cyst form of the organism, which are shed in the feces of infected humans & animals
Infection spreads from person to person and contaminated food & water.
Cysts become trophozoites in the intestine
Acute: abrupt cramping & frequent fould smelling stool

Question 17

Leishmaniasis

Answer 17

Transmitted by Phlebotomus sandflies (tropical)

Inoculation into skin, phagocytosed, become amastigotes, which reproduce within the macrophage.

Question 18

Localized Cutaneous Leishmaniasis

Answer 18

Ulcerating disorder
Leishman-Donovan bodies (macrophages filled with amastigotes)
Begins as a solitary papule, which erodes to form a shallow ulcer. Ulcers begin to resolve at 3-6 months, but healing may take a year or longer.
Diffuse cutaneous leishmaniasis develops in those who lack cell mediated responses

Question 19

Mucocutaneous Leishmaniasis

Answer 19

late complication of cutaneous leishmaniasis
Leishmania brazeiliensis
Rodents and sloths are reservoirs
A solitary ulcer appears, expands, resolves. Years later an ulcer develops at a mucocutaneous junction, highly destructive and disfiguring and erodes mucosal surfaces and cartilage.

Question 20

Visceral Leishmaniasis (Kala Azar)

Answer 20

Potentially fatal infection of the monocyte/macrophage system
Leishmania donovani
Localized collection of infected macrophages at site of sandfly bite, this spreads the organism throughout the mononuclear phagocyte system.
Normal organ architecture is gradually replaced by sheets of parasitized macrophages
patients become cachectic, massive splenomegaly.

Question 21

Trypanosoma cruzi

Answer 21

Chagas Disease- causes systemic infection
Flagellated
Transmitted from feces of insect that bites you, scratching the bite will promote contamination of the wound.
Divide rapidly in macrophages as amastigotes, which lose their flagella

Question 22

Acute Chagas

Answer 22

May cause fatal myocarditis

fatal cases: heart is enlarged and dilated, with a pale, focally hemorrhagic mycoardium

Question 23

Chronic Chagas

Answer 23

May lead to cardiac failure and GI disease
Develops years or decades after acute infection.
The organism is no longer present in the blood or tissue, infected organs have been damaged by chronic, progressive inflammation.
Extensive interstitial fibrosis, hypertrophied myofibers and focal lymphocytic inflammation, often involving the cardiac conduction system.
Megaesophagus, megacolon

Question 24

Congenital Chagas

Answer 24

Infection inutero leads to spontaneous abortion

Live births die of encephalitis within a few days or weeks,

Question 25

Trypanosoma brucei gambiense

Trypanosoma brucei rhodesiense

Answer 25

“African sleeping sickness”
Life-threatening meningioencephalitis
gambiense (chronic), rhodesiense (rapidly progressive)
Binary fission
Transmitted by blood sucking tsetse flies
**Humans are the only important reservoir

Question 26

African Sleeping Sickness

Primary Chancre

Answer 26

Papillary swelling topped by central red spot at site of innoculation
Subsides spontaneously

Question 27

African Sleeping Sickness

Systemic Infection

Answer 27

After appearance of chancre, blood stream invasion

Splenomegaly, “Winterbottom Sign” -enlargement of posterior cervical lymph nodes, myocarditis

Question 28

African Sleeping Sickness

Brain Invasion

Answer 28

Marked by apathy, daytime somnolence and sometimes coma.
Diffuse meningioencephalitis is characterized by tremors of the tongue and fingers, fasciculations of muscles, oscillatory movements of the arms, head, neck

Question 29

Primary Amebic Meningoencephalitis

Answer 29

Naegleria fowleri- free living in soil
Inoculated into nasal mucosa near cribiform plate
Invade the olfactory nerves, olfactory bulbs, then proliferate in the brain and meninges.
Brain is swollen & soft w/ vascular congestion and a purulent meningeal exudate
rapid progression of disease