Parasitic Diseases Flashcards
Define Paratism
The activity of an organism that spends any
portion of its life in direct contact with a host
species at the expense of the host
What are ectoparasites
- organisms that are found on the skin or only in the superficial layers of the skin.
- all ectoparasites are arthropods (invertebrates with a chitinous exoskeleton)
- fall into two main categories: insects (six-legged arthropods) and arachnids (eight-legged arthropods)
- insects such as lice, flies, and bedbugs
- arachnids such as mites, ticks, and spiders
What are Helminths?
– multicellular
– highly organised
– complex life cycles
What is Protozoa?
– exist in all body compartments
– intra and extra cellular
– Cause a spectrum of disease
– single-celled
- can be subdivided into 4 groups: Sarcodina (amebas), Sporozoa (sporozoans), Mastigophora (flagellates), and Ciliata (ciliates).
Describe the transmission of transmission of parasites
- Environmental / behavioral
– Associated with resistant cyst or ova - Giardia, Toxoplasma, Tapeworms, geohelminths
- Trichomonas vaginalis directness of contact precludes need for cyst formation
- Consumption of resistant stages with food
– The tissue cyst of Toxoplasma - Direct invasion
– Schistosomes and hookworms
List the 4 species of malaria
– Plasmodium falciparum
– Plasmodium vivax
– Plasmodium ovale
– Plasmodium malariae
* Falciparum malaria responsible for most deaths and severe disease
Describe the life cycle of malaria
What are the treatment options for malaria?
Chloroquine is the drug of choice for treatment of uncomplicated malaria caused by non-falciparum species in areas without chloroquine resistance.
Chloroquine kills the merozoites, reducing the parasitemia, but does not affect the hypnozoites of P. vivax and P. ovale in the
liver. These are killed by primaquine. Primaquine may induce severe hemolysis
in those with G6PD deficiency
Uncomplicated, chloroquine-resistant P. falciparum infection is treated with either Coartem (artemether plus lumefantrine) or Malarone (atovaquone and proguanil
the artemisinins, such as artesunate or artemether, are widely used in combination with other antimalarial drugs.
What is the epidemiology of malaria?
It occurs primarily in tropical and subtropical areas, especially in Asia, Africa, and Central and South America
What are the Mechanisms of pathogenesis?
- Disruption of normal physiological function
– Giardia: uptake and metabolism of bile induces malabsorption - Invasion of host tissues
– Disruption of metabolism: trypanosome induced cardiac failure
– Disruption of host immune responses - Toxoplamsa & Leishmania invasion of macrophages
- Physical presence
– Plasmodium aggregation in cerebral malaria, Ascaris blockage of gut - Induction of immune responses
– Leishmania lesions associated with protective immune response
– Toxoplasma encephalitis associated with cyst reactivation
– Schistosome granuloma formation
what are the three major pathogens of Trypanasoma?
what diseases do they cause
Trypanosoma cruzi - chagas disease
Trypanosoma (brucei) gambiense, and Trypanosoma rhodesiense (brucei) - sleeping sickness
How do trypanasoma species affect host cells.
When the bug bites, the site is contaminated with feces containing trypomastigotes, which enter the blood of the person (or other reservoir) and form nonflagellated amastigotes
within host cells. Many cells can be affected, but myocardial, glial, and reticuloendothelial cells are the most frequent sites.
Describe the life cycle of Trypanosoma cruzi
SCHISTOSOMA
trematodes
Schistosoma species (Schistosoma mansoni
and Schistosoma japonicum) adults live in the mesenteric veins, whereas S. haematobium lives in the veins draining the urinary bladder. Schistosomes are therefore known as blood flukes.
Schistosoma mansoni and Schistosoma japonicum affect the gastrointestinal tract,1
whereas Schistosoma haematobium affects the urinary tract.
What is the immune response for schistosomas
Most of the pathologic findings are caused by the presence of eggs in the liver, spleen, or wall of the gut or bladder. Eggs in the liver induce granulomas, which lead to fibrosis, hepatomegaly, and portal hypertension.
The damage is due both to digestion of tissue by proteolytic enzymes produced by the egg and to the host inflammatory response that
forms granulomas in the venules.The eggs of S. haematobium in the wall of the bladder induce granulomas and fibrosis, which can lead to carcinoma of the bladder. The granulomas are formed in response to antigens secreted by the eggs.
Schistosomes have evolved a remarkable process for evading the host defenses. There is evidence that their surface becomes coated with host antigens, thereby limiting the ability of the immune system to recognize them as foreign.
what pathogen causes Toxoplasma?
The life cycle of toxoplasma?
Toxoplasma gondii
The definitive host is the domestic cat and other felines; humans and other mammals are intermediate hosts.
The cycle within the cat begins with the ingestion of cysts in raw meat (e.g., mice). Bradyzoites are released from the cysts in the small intestine, infect the mucosal cells, and
differentiate into male and female gametocytes, whose gametes fuse to form oocysts that are excreted in cat feces.
Infection of humans begins with the ingestion of cysts in undercooked meat or from accidental contact with cysts in cat feces. In the small intestine, the cysts rupture and release forms that invade the gut wall, where they are ingested by macrophages and differentiate into rapidly multiplying trophozoites (tachyzoites), which kill the cells and infect other cells
Cell-mediated immunity usually limits the spread of tachyzoites, and the parasites enter host cells in the brain, muscle, and other tissues, where they develop into cysts in which the parasitesmmultiply slowly. These forms are called bradyzoites.
Clinical presentation of toxoplasma
- Acute infection
– Asymptomatic / mild
– Rarely: severe chills, fever, myalgia,
lymphadenopathy, fatigue - Reactivation disease
– Retinochorioditis, mental statu - Congenital infection
– Chorioretinitis, hydrocephalus, convulsions,
intracerebral calcification
Clinical presentation of Leishmania
Cutaneous lesion
Visceral, mucocutaneous and cutaneous disease
Disfiguring granulomatous, ulcerating lesions destroy nasal cartilage but not adjacent bone
Describe filarial worms and the diseases they cause
- Long lived
- Require larval passage through insect vector
- 4 major species
– Lymphatic disease: - Wucheria bancrofti, Brugia malayi
– Blindness: - Onchocerca volvulus, Loa loa
Describe the Pathogenesis of gut parasites
Intestinal mucosal injury
– spectrum normal mucosa to subtotal villus atrophy
– microvillus damage throughout spectrum
– damage correlates to functional impairment
Luminal factors
– nutritional competition
* B12 theft - Ascaris
– barrier to adsorption
* parasite & bacterial overgrowth
– disruption of normal gut physiology
* bile salt deconjugation in giardiasis
– obstruction
Describe the transmission of parasites
Cysts and ova
– Resistant structures
– May require period of development before becoming infective
– Release of next stage as a result of environmental triggers (eg stomach pH)
– Facilitates transmission between hosts
Larval invasion
Contamination of
– Water supply/ environment
– Food sources
* Cleaning
* Irrigation
* Inadequate cooking
* Faecal – oral transmission
what causes Protozoa: Giardiasis
Direct life cycle
Pathogen = Giardia lamblia
Transmission = ingestion of cysts (Faecal oral route)
- fecally contaminated food and water
Clinical Findings
- Watery (nonbloody), foul-smelling diarrhea
-nausea, anorexia, flatulence, and abdominal cramps
Significant morbidity in: Children & Immunosuppressed
Describe Protozoa: Ameobiasis
Pathogen = Entamoeba histolytica
Epidemiology = worldwide distribution, most frequently in tropical countries
Transmission = ingestion of cysts that are
transmitted primarily by the fecal–oral route
Pathogenesis = Passage via the portal vein leads to damage to liver
– invasion of intestinal mucosa
– dissemination to other organs
Clinical Findings:
– asymptomatic (E. dispar)
– colic, frequent bowel movements
– dysentary
– disseminated disease
Helminths: Ascaris lumbricoides
Ascaris lumbricoides causes ascariasis
Epidemiology = World wide distribution
Transmission = ingesting worm eggs in food or water contaminated with human feces
Pathogenesis = The eggs hatch in the small intestine, and the larvae migrate through the gut wall into the bloodstream and then to the lungs and are swallowed.
Clinical findings:
– larvae: pulmonary migration
* Cough, fever, wheezing
– Adults: gut
* Disruption & obstruction
* Malnutrition
* B12 deficiency
Helminths: Hookworms
Pathogens = Ancylostoma duodenale (Old) and Necator americanus
Transmission = when filariform larvae in moist soil penetrate the skin
Pathogenesis = They are carried by the blood to the lungs, migrate into the alveoli and up the bronchi and trachea, and then are swallowed. They develop into adults in the small intestine, attaching to the wall. They feed on blood from the capillaries of the intestinal villi.
Clinical manifestations:
– At skin – itchy papules
– In gut
* Iron & protein loss
– Migration through lungs
* Pneumonia with eosinophilia
Helminths: Trichuris trichuria
Trichuris trichiura causes whipworm infection (trichuriasis).
Transmission = infected by ingesting worm eggs in food or water contaminated with human feces
Epidemiology = Warm humid climates
Pathogenesis = The eggs hatch in the small intestine, where the larvae differentiate into immature adults. These immature adults migrate to the colon, where they mature,
mate, and produce fertilized eggs, which are passed in the feces.
Clinical findings:
– Bloody diarrhoea – no fever
– Rectal prolapse
– Anaemia
– Wasting
– Eosinophilia
Helminths:Tapeworms
There are two important human pathogens in the genus Taenia: T. solium (the pork tapeworm) and T. saginata (the beef tapeworm).
- Disease associated with migration of larval stages
– significant cause of epilepsy
