Protozoal Infections Flashcards
Malaria
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
Plasmodium falciparum
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
Plasmodium malariae
Mild form of Malaria
Least common agent
Broad geographical distribution
Plasmodium vivax
Common agent of Malaria infection
Rare in Africa, bc population lacks the proper receptor on their RBCs
Babesia
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
Toxoplasmodium gondii
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
Toxoplasma Lymphadenopathy
Occurs in immunocompromised patients
Usually resolves spontaneously in several weeks to months
Congenital Toxoplasma Infections
Primarily affect the brain
Infection in the fetus is more destructive than in postnatal infection
Necrotizing meningioencephalitis
Fetal infection often leads to spontaneous abortion
Toxoplasma Encephalitis
Immunocompromised hosts
Most cases reflect reactivation of latent infections
Brain is most commonly affected and produces a multifocal necrotizing encephalitis.
Fatal if not treated
Entamoeba histolytica
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
Amebiasis Amebic Trophozoite Stage
Found in stools of patients with acute symptoms
Trophozoites sometimes contain phagocytosed RBCs
Develop into cysts- non-motile, form glycogen masses and chromatoidal bodies
Amebiasis Amebic Cystc
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.
Intestinal Amebiasis
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
Amebic Liver abscess
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
Cryptosporidiosis
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
Giardia lamblia
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
Leishmaniasis
Transmitted by Phlebotomus sandflies (tropical)
Inoculation into skin, phagocytosed, become amastigotes, which reproduce within the macrophage.
Localized Cutaneous Leishmaniasis
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
Mucocutaneous Leishmaniasis
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.
Visceral Leishmaniasis (Kala Azar)
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.
Trypanosoma cruzi
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
Acute Chagas
May cause fatal myocarditis
fatal cases: heart is enlarged and dilated, with a pale, focally hemorrhagic mycoardium
Chronic Chagas
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
Congenital Chagas
Infection inutero leads to spontaneous abortion
Live births die of encephalitis within a few days or weeks,
Trypanosoma brucei gambiense
Trypanosoma brucei rhodesiense
“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
African Sleeping Sickness
Primary Chancre
Papillary swelling topped by central red spot at site of innoculation
Subsides spontaneously
African Sleeping Sickness
Systemic Infection
After appearance of chancre, blood stream invasion
Splenomegaly, “Winterbottom Sign” -enlargement of posterior cervical lymph nodes, myocarditis
African Sleeping Sickness
Brain Invasion
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
Primary Amebic Meningoencephalitis
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
