AI generated exam 2
Definitive host is vertebrate, asexual in both vert and invert
Phylum euglenozoa:
Class kinetoplasta
Order: trypanosomatida
Kinetoplast no cyst heteroxeneous
Vertebrate host blood and lymph
Invertebrate host gut (blood feeder)
Promastigote and epimastigote (both troph)
Promastigote found in leishmania (extracellular) (invert host): longer and slender, NO undulating membrane, 1 anterior free flagella, anterior kinetosome, anterior kinetoplast
Epimastigote in the trypanosoma also in invert host, extracellular form: short undulating membrane, kinetoplast anterior to nucleus but more to the midpoint of the troph.
Trypomastigote: in trypanasoma, long undulating membrane, kinetoplast posterior to the nucleus found in the vertebrate host. Extracellular form
Amastigote: circular form, interior flagella, intracellular, family is leishmania and trypanosome. Anterior kinetoplast, found in vertebrate host
Leishmania intermediate host: the sandfly, south and central america
Vectors:
Phlebotomus: old and new world infection
Lutzomyia: central and south america
Cutaneous Leishmaniasis:
Leishmania tropica and leishmania major
Mostly phlebotomus
Leishmaniasis stays in skin, attacks reticuloendothelial cells
Gerbils serve as a reservoir host of Leishmania tropica and leishmania major
Incubation is a few days to a few months
Multiplies in the mid gut of the sand fly
Symptoms/ pathology: open sore size of a quarter, main pathology
Transmission primarily due to sand fly bites, touch/flies
Treatment is pentastam
, in some areas there are vaccines for prevention in the middle east, only effective for the cutaneous form.
Diagnosis is a skin scrape amastigotes
Mucocutaneous:
Found more in south and central america
Leishmania brazilense
Phlebotomous and lutem
RE cells in mucosal layers, found in mouth, nose pharynx, cartilage and ears
Lifecycle: the same except, promastigote multiplies in the hind gut of the fly
Reservoir species are sloths and anteaters
Symptoms and pathology:
Initially starts with red papule on the skin, itchy and can ulcerate, can heal in 6-15 months
Secondary legion, typically in mucosal layers, nasal or buccal, can cause degeneration of cartilage and soft tissues.
Diagnosis: scrape and culture
Treatment pentastam.
Visceral Leishmaniasis:
Leishmania donovani, dum-dum fever, kala-azar
Sir william discovered it in india
Found in the RE cells of the liver and the spleen.
Symptoms and pathology: headache, fever, chills, leads to bleeding of mucous membranes, diarrhea or dysentery sometimes asymptomatic.
Incubation is 10 days to a year, on average 2-4 months.
Pathology: wasting, anemia, enlargement of the liver and or spleen, abdominal discomfort and abdominal swelling
Death in 6 months-2 years
Diagnosis: biopsy of liver or spleen. ELISA
Tissue becomes hyperplastic or brittle can be dangerous. Can lead to hemorrhaging due to biopsy.
treatment : trivalent and pentavalent, amphotericin B
Post kala-azar symptoms: if not treated properly pustules on the skin mostly on the face. Large red rash with pustules across the face
90-99% will die if untreated.
Leishmania mexicana:
Can do cutaneous, mucocutaneous and visceral
Most of the time presents as cutaneous or mucocutaneuous
Chickero’s ulcer is the ideological agent. Found in central america, has been found in texas.
Reservoirs are rodents. Lesions can last for 40 years
Genus Trypanasoma:
Vector is tsetse flies (high rate in the fly belt) (genus is glossina)
Heteroxeneous parasites. Vert host-> definitive hosts
Arthopod as intermediate host.
Two groups based on how they infect definitive host:
Anterior station: arthopod passes parasite through bites
Posterior station: develop in hind gut of the vector, transmitted through feces
Trypanasoma brucei Rhodesiense:
Causes acute African Sleeping sickness fatal within a year
Native reservoir hosts, typically native game animals
Short term infection due to higher pathogenicity.
Vector is glossina
Symptoms associated: intermittent fever, swollen lymph nodes (swelling referred to as winter bottoms), sore at bite site in some cases,
Central to east africa.
Trypanasoma brucei gambiense:
More chronic form, less pathogenicity, lower fatality rate
West and central africa
Vector glossina
Symptoms: sore at bite site in some cases, swollen lymph nodes, enters CNS-> neurological problems.
Phase 1: incubation, tryp in the skin, travel in upper vasculature. Painful red lesion at bite site, inflammation around the site, occurs for 1-2 weeks
Phase 2: tryp in circulation, fever, headaches, skin rashes, duration for this is variable
Phase 3: Collecting in lymphatic nodes and channels, leads to irritation, swelling and proliferation of epithelial swells, leads to enlargement of the lymph nodes, fever, headache delayed sensation of pain. General weakness.
Phase 4; impact on other sites, movement to CNS more typical of gambiense, Mental dullness (apathy, slower to react, issues with coordination, seizures), with Rhodesiense typically more impact on the heart (decrease effectiveness of heartbeat), decrease in weight loss overall, increased drowsiness-> coma-> death
Byproducts of parasite are toxic and circulate in blood stream. Leads to encephalitis, hallucinations, variable antigen types, -> host body will lyse own RBC.
Trypanosoma brucei brucei: E.A of nagana.
Same life cycle as others, just found in native ruminants, and a few other animals, not pathogenic for native species, affects non native bovine.
Symptoms: anemia, fever, water eyes and nose, severe weight loss.
Diagnosis of Trypanosoma: blood smear looking for slender trypomastigote stage, lumbar puncture, ELISA.
Treatment:not as toxic older drug of choice is suramin (not effective if they have reached CNS), Melarsopranol -toxic to CNS form however it is dangerous can cause vomiting and kidney damage, current drug of choice is ornidyl (tolerated better) effective at CNS, more expensive less effective against Rhodesiense.
Control: eliminate the tsetese fly, remove vegetation from the outside of homes, pan african tsetse and trypanasomiasis eradication campaign, shooting game animals
Posterior station trypanasomes:
Trypanasoma Cruzi:
Ediological agent of chaga’s disesase, AKA South American Sleeping sickness
Many wild and domestic animals serve as reservoir species.
Very distinct C shape trypamastigote.
Intermediate host: kissing bugs 28+ species (reduviid bugs)
Triatoma spp.
Panstrongylus Spp.
Transmission occurs through feces of the kissing bug.
Life cycle in humans:
Stage 1:
tryp enters in peripheral circulation through a bite from a kissing bug near the mouth or eyes. An edema forms, if around the eye or cheek can swell and close the eye known as “romanas eye”. If around the mouth a red papule develops itchy and uncomfortable. Headache and fever accompany this as well. Some weakness develops as well. Lasts 1-3 weeks or longer
Stage 2:
Tryp finds cells and begins entering. Symptoms from phase 1 subside unless reinfected.
Stage 3:
Amastigote damage, tryp’s begin reproducing and bursting cells. Edema around the cells and tissues develop, some lymph node infiltration, some inflammation in the lymphatic system.
Acute and a chronic phase.
Acute seems to be in 5 or under and chronic tends to be older children. Acute is more pathogenic Large immune response to the pseudocysts. The large immune response to pseudocysts triggers an inflammatory response. Can lead to large numbers of neighboring cell death. When in cardiac tissues, swelling, death of cardiac nerves which leads to weakening of the cardiac muscles, which can lead to heart failure.
Anemia weakening and the loss of strength, chills and intermittent fevers which coincide with the bursting of cells. Nervous disorders if it reaches the CNS.
Chronic form:
Swelling and weakening of the heart, cardiac failure. Central and peripheral nervous system disruption. Interruption of the digestive system due to infiltration of gut musculature, decreased peristalsis. Swelling of the esophagus and the colon.
Diagnosis:
Looking at tissue samples and finding pseudocysts. Blood or lymph smears, Immuno diagnosis using fluids that may contain antigens (cross reactive with leishmania), xenodiagnosis (feeding sterile bugs with infected blood) looking for infected blood.
Treatment:
Suramin if in the blood system
Benznidazole and nifurtimox for acute
Reduviid control, use of pesticides and preventing infection, using mosquito nets and bug sprays.
Trypanosoma equiderm:
Horse trypanasome
E.A of dourine
Sexually transmitted in horses, donkeys and mules.
No arthropod vector. Found in areas of africa, asia southern and eastern europe, russia and mexico.
Phase 1: transmitted through fluids in sexual contact, symptoms in genitalia, edema in genital tissue, discharge from the vagnia or the urethra or both. Deep pigmentation of the genital region.
Phase 2: rashes on the sides of the body.
Phase 3: paralysis, begins with neck, face and then the hind body can lead to death.
Diagnosis: looking at blood smear, seminal smear, vaginal smear. Complement fixation test (looking for complements and antigens specific to pathogen).
Treatment: version of suramin not very effective. Any positive horses are euthanized.
Plasmodium:
Phylum: apicomplexa
Most species are parasitic.
Have an apical complex: only able to be seen through electron microscopy
Reproduction: sexual and asexual reproduction Multiple fission is their form of asexual reproduction. Division of nucleus first, then cytokinesis. Sexual reproduction: a set of microgametes (sperm) and then a macrogametes (egg). They are diploid as microgametes and macrogametes and then haploid for a majority of their life cycle.
Class Aconidasida:
Order: Haemosporidia (blood spores)
Heteroxeneous: circling between arthropod vector and vertebrate. Merogany in vertebrate host and typically fertilization and sporagomy in arthropod host. Arthropod is the definitive host, humans are the intermediate host.
Genus: Plasmodium
E.A of malaria.
Number 1 parasitological killer in the world, oldest documented species
Definitive host: Anopheles mosquito.
Symptoms:
Paroxysms( periodic fever associated with chills). Periodicity ranges from 24-48-72 hours.
Chills are about 1 hour, then perfuse sweating which lasts 2-4 hours. Individuals might go undergo nausea, vomiting and intense headaches typically lasts about 10 hours, fever can be as high as 106.
Tertian-48 hour
Quartan- 72 hour
Plasmodium Vivax:
E.A of benign tertian malaria:
Less pathogenic than other malaria
43% of all cases of malaria. Found in temperate zones as well as tropical.
Currently most common cases are found in asia and north africa.
Only infects red blood cells.
Causes enlargement of RBC. Causes schuffner's dots.
Ring trophs in RBC round gametocytes.
Relapse can occur due to merozoites in the liver within 1-8 years.
Plasmodum faliciparum:
Deadliest Malarial species.
E.A of Malignant Tertian malaria
Causes 50% of global cases. 25% of cases are fatal. Tropical and subtropical.
Infects RBC of all ages.
Infected RBC become sticky.
Can cause cerebral malaria
No enlargement of RBC, no dot morphology.
Cytoplasm develops mauries cleft
Recrudescence 1-2 years: recurrence due to merozoites in low levels in RBC.
Blackwater fever (sign of recrudescence) : Urine has gone dark
Plasmodium Malariae:
E.A of quartan malaria
Africa, india, europe, brazil and panama
Older RBC
6% of cases
Recrudescence: merozoites in RBC can last up to 53 years.
Trophs are more band shaped than ring shaped.
Plasmodium ovale:
E.A Mild tertian malaria
Rarest infective plasmodium
Found in africa, india, the philippines and vietnam
Found rarely in europe and the US
Relapse into liver Cryptozoite and hypnozoites.
Pathogenicity of malaria:
Host immune response leads to fever, chills,headaches etc etc
Anemia
Host autoimmune issues due to release of endotoxins from RBC higher incidence with falciprum
Loss of O2 to tissues and cells, can cause cell and tissue death
Accumulations of iron pigmentation can cause cell and tissue functioning disruption. Which can shut down kidneys
Often get host inflammatory response
For plasmodium falciparum, cerebral complications
Severe headaches, comas, hypoxia, psychotic tendencies.
Pulmonary edema
Algid malaria (circulatory shock due to drop in body temp)
Diagnosis of Malaria:
Blood smear, antigen and PCR tests
Historical Impacts:
Contributed to the fall of several empires. (greek and roman empires), 323 BC potential killer of alexander the great. Minimized the spread of colonization in some parts of west Africa. In the 1800’s 20-40% of individuals admitted in New orleans had malaria. Decline of malaria in the U.S: conversion of land.
Host resistance:
Plasmodium vivax: because they are the most common type of malaria there is more resistance to it.
Duffy blood groups
Enters cell through receptor mediated endocytosis.
Three alleles responsible
Fya and Fyb produce proteins that vivax uses. They are codominant alleles. If individuals have either of them they are vulnerable
Fy is recessive and codes for no proteins, leading to a resistance to the parasite. 54% of african americans are homozygous recessive for Fy.
Sickle cell:
Response to falciforom.
A allele for sickle B for concave (normal) morphology
AA-> sickle cell-> lower fitness
AB-> co-dominant both types-> if in endemic malaria area they have higher fitness
BB-> normal-> endemic lower fitness Nonendemic higher fitness.
Protective immunity to super infection: unable to be infected with a different plasmodium.
In endemic areas infants develop resistance from their mothers.
Control:
Controlling the vector, eliminate definitive host by eliminating breeding sites, insecticides
Biological control: Gambusia: mosquito fish, transgenic mosquitoes: refractory (unable to transmit disease prevents invasion of gut cells)
Treatment:
quinine tree compounds disrupt the erythrocytic cycle, interrupts merogamy, not effective to sporozoites or exoerythrocytic
Chloroquine: non resistance malaria treatment, now developing resistance. No adverse side effects, impacts sporozoites and erythrocytic stages
Primaquine: more toxic, acts on any type of exoerythrocytic forms
Mefloquine: good for resistance, impact all life stages. Lots of side effects
Tafenoquine: vivax and ovale. If there are hypnozoites.
Vaccines: testing since 2019, reduce the risk of contracting malaria by 40%, risk of serious illness-> 30%
Administer 3 doses block parasite from infecting liver
Natural control: mosquito dying from infection
Leucocytozoon genus (aconodistida):
Bird hosted
Domestic and wild bird.
Problematic in turkey and ducklings
Leukocytozoa Simondi: typical in poultry
Young waterfowl-> 85% fatality rate
Individuals develop anemia and develop large livers. Liver tissue becomes necrotic
Can kill a duckling in less than a day. Only has exoerythrocytic merogamy. Vectored by black flies.
Haemoproteus Genus:
Also undergo exoerythrocytic merogamy
Birds and reptiles.
Vectored by biting midges.
Other apicomplexans:
Class conoidasida, associated with the apical complex, cone of fibroid structures.
Encapsulated sporozoites within sporocysts.
Sporocysts occur outside of the host, usually in the environment.
Oocyst leaves with feces when it leaves unsporulated in environment then it sporulates and goes through sporagamy. Leaves an oocyst zygote and undergoes sporulation and develops into a haploid sporocyst.
Eimeria:
Can have 4 sporocysts and 8 sporozoites
Monoxeneous
Host tissue, site specific
Hosted by fish, skates sharks, lizards, mammals and birds.
After 3 generations of merogamy, self limits and stops reproducing.
E. tenella-> pathogenicity is bloody diarrhea, sloughing of epithelium
Control and prevention: keep birds away from feces. (slotted floor)
Dosing with few oocysts as a “vaccine”
Prophylaxis in feeds.
Good hygiene in coops.
Diagnosis: oocyst in feces.
Toxoplasma:
2 sporocysts and 8 sporozoites
Toxoplasma gondii
Human health and veterinary importance.
E.A of toxoplasmosis
Heteroxeneous omnivore and herbivore. Sexual reproduction in cats. Humans are intermediate hosts.
Symptoms/pathology:
Acute and chronic phase.
Acute(if immune system does not suppress the effect): Rapid division destroys host cells by undergoing merogamy and bursting cells.
Symptoms: swollen lymph nodes, fever, headaches, muscular pain, pulmonary complications, anemia, death in young or immunocompromised individuals.
Caused by fecal contamination with sporulated oocysts from an infected animal (cats, mice). Can also be transferred from uncooked meat such as beef and pork
Chronic (immune system suppression):
Often asymptomatic
Symptoms are associated with the death of bradyzoites.
In cerebral infections this can cause death of nerve cells which are replaced by glial cells
If it reaches the retina it can cause some blindness, zoidocysts bursting can cause blindness if happens in eye as well.
Myocarditis if it happens in the heart
Diagnosis: PCR, biopsy and ELISA.
Treatment: Pyrimethamine and sulfonamides, interrupt folic acid synthesis.
Spiramycin if pregnant, inhibits protein synthesis
Atovaquone-> impacts zoitocyst mitochondrial membrane
Can manipulate host behavior, mice no longer run from cat urine, generally less anti prey behavior.
Sarcocystis:
4 sporocysts and 8 sporozoites.
Heteroxeneous cycles between carnivorous(definitive) and herbivorous (intermediate)
Rice breast (duck)
Lifecycle:
Herbivore consumes a sporocyst through fecal contamination, it then releases sporozoites, they leave the intestines into other cells, they go through merogamy, burst the cell and then form zoitocysts. Found in skeletal and cardiac muscle, also found in cerebral. Waits for definitive host to consume the intermediate and they then release bradyzoites. Bradyzoites go through merogamy, gametogamy and then sexual reproduction.
Gregarinasa (subclass of aconidasida)
Parasites of invertebrates. They do not go through merogamy, gametocytes are extracellular. Typically monoxenous and host specific, found in gut or repro organs of host.
Monocystis Lumbricus:
Found in seminal vesicles of earthworms
They consume the sporulated oocyst-> sporozoites are released into the gut-> they move out of the gut to the seminal vesicles.