Lifecycles Flashcards
Whipworm
Trichuris trichura
Class: Metazoan nematode
Direct cycle (1 host= human, mainly, can be found in other animals rarely) Human= definitive host
Both extracellular and intracellular depending on the stage
1) Embryonated eggs found in contaminated food/water ingested
2) They go intestine, and hatch as larvae there:
L1 stage. intracellular enters epithelia
L2: forms a tunnel
L3/L4: partly intracellular partly extracellular
3) Then it develops to adults in the cecum, takes like 3-4 months
4) Females start laying eggs, 30.000 a day, adults can live up to 1-8 years
5) Eggs are released as unembryonated from feces
6) It develops to two-cell stage + advanced cleavage + embryonated egg stage in soil.
Diagnosis: egg check stool microscopy
Pathology: cause disease depending on egg burden/host defense
Can cause malnutrition, or evolve into dysentery syndrome in worst cases
Strongyloides stercoralis
Class: Metazoan nematode
Direct cycle (often also dogs can be hosts though)
1) The rhabiditiform larvae in the intestine are excreted from stool + they mature to free-living forms
2) Sexual reproduction occurs in soil, females secrete eggs
3) Rhabditiform larvae hatch from eggs in environment, then they become flariform
4) Flariform female larvae penetrate the skin of host, and goes intestine, maturates into adult female (no reproduction= parthenogenesis)
5) then eggs are produced, which develops into flariform again to drive autoinfection - or some goes to stool and continues the cycle
Diagnosis:
check stool w microscopy for larvae: golden standard but low efficiency: because only 40 eggs produced per day
IgG ELISA + serology (can stay positive for long + cross-reactivity issues) /PCR/ endoscopy + biopsy
Symptoms:
Pathogenecity caused by flariform larvae
Rash, lung irritation, cough, diarrhea, GI complaints, can go chronic or cause hyperinfective syndrome in immunocompromised
Classification
Metazoan: multicellular
Protozoan: unicellular
Nematode: roundworm
Trematode: fluke/flatworm
Cestode??
Hookworm
A. duedonale/Necator americanus
Class: metazoan nematode
extracellular direct cycle
1) Eggs are secreted by humans, rhabditiform larvae hatches (2 days), develops into filariform in environment
2) Flariform larvae penetrate the skin/barefoot
3) Larvae swallowed, goes bloodstream/intestine, ends up in lungs at the very end: coughed and swallowed again, then goes back to the intestine (lung to intestine takes 1m to travel)
4) In the small intestine, two larvae meet and develop into adult larvae
they attach to the mucosal wall using their teeth, also feed for maturation
5) larvae sexually reproduce, can stay there for 2 years if untouched
Diagnosis: check eggs in feces microscope
Need to analyse them fast, light infections cannot be detected at all, concentration treatment can be done
Pathology:
rash on skin, cough sore throat from flariform larvae, abdominal pain, diarrhea, weight loss from adult
Schistosoma
Class: metazoan trematode (fluke/flatworm)
Indirect cycle /snail intermediate host
Most important ones: S.mansoni, S.japonicum, S.hametobium
1) Eggs are released from humans depending on species: S.mansoni and japonicum on feces, S. hametobium on urine
2) Eggs hatch and release miracidia
3) Miracidia moves and goes to penetrate snail, infects the snail
4) in snail replication happens asexually, oocysts explode and release sporocysts
5) free-swimming cercaria released in water, swims around and finds human
6) penetrates human skin, cercaea loses its tail, and migrates to lung heart liver, then depending on species: goes to
-S.japonicum/mansoni: bowel
-S. hametobium: bladder
7) sexual reproduction romantic: release eggs females
Diagnosis : check eggs in urine/feces, need centrifuge to find eggs better
quantifying can be done
Adult worms can live up to 30 years
PCR / Adult worms: CCA/CAA Ag-test
Pathology: response to eggs, eggs get stuck in tissues
eggs on tissues cause granuloma
Katayama fever (acute schisto) on travelers
GI bleeding + liver failure (eggs destroy the liver and kidneys, swelling)
Malaria
Plasmodium: P.vivax, P.falciparum, P.malariae, P. knowlesi, P.ovale
Indirect cycle/also involves mosquitos
Protozoan intracellular parasite
1) malaria-infected female Anopheles injects sporozoites to humans
2) Sporozoites infect liver cells and mature into schizonts, which rupture and release merozoites. = Liver stage
3) Merozoites infect red blood cells. The ring stage trophozoites mature into schizonts, which rupture releasing merozoites.
4) Some parasites differentiate into sexual erythrocytic stages (gametocytes). Blood stage parasites are responsible for the clinical manifestations of the disease.
Insect cycle
5) The gametocytes, male (microgametocytes) and female (macrogametocytes), are ingested by mosquito.
6) While in the mosquito’s stomach, sexual reproduction happens: forming ookinete in the stomach
7) midgut: sporozoites multiply and form oocysts. The oocysts grow, rupture, and release sporozoites, which make their way to the mosquito’s salivary glands.
Diagnosis: check blood under microscope w staining = golden
ELISA measures past infections
Pathology: Uncomplicated: Fever Chills Sweats Headaches Nausea and vomiting Body aches General malaise
Complicated: Cerebral malaria, with abnormal behavior, impairment of consciousness, seizures, coma, or other neurologic abnormalities
Severe anemia due to hemolysis
Acute kidney injury
Hyperparasitemia, where more than 5% of the red blood cells are infected by malaria parasites
Leishmania
Class: protozoan intracellular
Indirect cycle, can also involve other reservoirs
More than 20 species can infect humans
Causes 3 types of disease: Cutaneous (skin): L.major, L.tropica
Visceral (organ): L.infantum, L.donovani
Mucosal: L. braziliensis
1) Sandfly takes a blood meal and injects promastigotes
2) Promastigotes are phagocytosed by phagocytes, there they turn into amastigotes: they are stronger, they don’t have flagella = survive inside phagocytes
3) Amastigotes multiply in immune cells and explode: then infect other cells
4) Sandfly takes blood meal, ingests phagocytes infected w amastigotes
5) Phagocytes ingested, amastigotes turn into promastigotes, they multiply and move to salivary gland
Obligated parasite: needs host to survive
Other reservoirs: rodents, dogs, gerbals> carriers
Intracellular parasite
Incubation time: 2 weeks – 6months (up to years) (from bite)
Result: immune deficiency -> can lead to death
Diagnosis: PCR*,detect parasites in tissues, or rapid Ag test also available
Guinea worm
Dracuncula mediensis
Class: metazoan nematode extracellular
Indirect cycle
1) human either eats foods contaminated with copepods/drinks unfiltered water
2) Larvae released inside human when copepods die, larva penetrate host stomach, they mature in subcutaneous tissues, then sexually reproduce
3) Male dies after sex lol (3-7 months) female grows and goes back to the feet skin to leave out from feet, also releasing larvae. It takes almost 1 year for it to leave.
4) Released larvae to water is consumed by copepod, and ingested again.
Almost eradicated
Diagnosis:
Causes disgusting this thing, it also hurts, gets swelling, and can disturb up to a year -chronic-, sometimes causes allergy
No treatment, just filter the water, they wrap it around a rod once its coming out
Trypanosoma cruzi
trypomastigotes: infect
epimastigotes: replicate
Class: Intracellular flagellated protozoa
- causitive agent Chagas disease
- acute phase: (asympt), fatigue, fever, vomiting, diarrhae
- chronic phase: (asympt), GI-complication, cardiac complications
- indirect life stage
Transmission: Triatomine Bug: Kissing bug: bloodmeal, injection of metacyclic trypomastigotes which penetrate cells at the bite site (intracellular). Here they transform into amastigotes which further multiply via binary fission. The amastigotes develop into trypomastigotes and burst out the cell and go into the blood circulation, and are able to infect new cells (transform into amastigotes; cycle repeats). The kissing bug is able to take up trypomastigotes during a bloodmeal. The trypomastigotes > epimastigotes > multiply in midgut > metacyclic in hindgut > passes parasite to host via feces that enter the bite wound (accidently)
- Other reservoirs: dogs, rodents, raccoons
- other transmission route: consumption of uncooked food or beverages that are contaminated with T. cruzi, blood transfusions, congenital transmission, organ transplants, laboratory accidents
Diagnosis: depends on stage of infection
- acute phase: detect parasites in bloodstream via microscopy, molecular diagnosis and PCR
- chronic phase: detect antibodies against parasite via serological testing (ELISA, immunoblot, IFA)
Cryptosporidium (pool one)
Protozoan Infects: Humans and animals Direct lifecycle C. hominis, C. parvum “Intracellular” • Target epithelial cell digestive tract • Microvilli lengthening, flattening and fusion to surround the parasite
• Oocyst (sporulated) exit host via feces, here it remains infectious 6-8 months and can survive in harsh conditions (temp)
• Transmission: contaminated water/food
1) Ingestion
2) Oocyte releases sporozoites (excystation)
3) Sporozoites infect epithelial cells of GI (trophozoite) and asexual multiplication happens -> merozoite
4) Sexual cycle: multiplication producing microgametes(male) and macrogamonts (female)
5) Fertilization of macrogamonts by microgametes (rupture from macrogamont) = zygote
6) Zygote forms two types of oocysts (sporulation)
-Thin-walled: involved in auto-infective cycle
-Thick-walled: excreted into the environment
Diagnosis: detection of thick-walled cysts in feces
Acid-fast staining
Immunofluorescence microscopy
PCR
Symptoms: some are asymptotical
Symptoms 2-10 days pi, self-limiting (except immunodeff)
Damage GI: malabsorption
Diarrhea, cramps, dehydration, nausea, vomiting, fever, wasting
Trypanosoma brucei
hemoflagelated protozoan
- extracellular life stage
- T. b. rhodesiense (acute), T. b. gambiense (chronic)
- Indirect cycle
- transmission of metacyclic form to human host during bloodmeal of infected tsetse fly (indirect lifecycle). Metacyclic form differentiates in bloodstream to bloodstream form (BSF). In the blood stream they replicate via binary fission. Eventually, the parasites crosses the BBB and reside in the CSF (neurological symptoms).
The parasite is ingested by the Tsetse fly during a bloodmeal, here they differentiate into the procyclic form in the midgut and leave the midgut to the salivary gland (epimastigotes), here they multiply first and differentiate into non-replicative metacyclic trypomastigotes.
Reservoirs: mammals, domestic cattle, ungulates, primates
Symptoms:
- chancre at site of inoculation
- haemolymphatic stage: non-specific: fever, lymphadenopathy
- meningoencephalitis: neuropsychiatric manifestations: sleep disorders
Diagnosis: early diagnosis is difficult due to non-specific symptoms
- Rapid diagnostic test (antibody detection): passive screening and surveillance (gambiense) only
- molecular detection: no nucleic acid-based tests are validated for diagnosis
- Light microscopy blood and CSF: both gambiense and rhodesiense (invasive): examined for motile parasites, and blood smears should be fixed
Giardia intestinalis
Important:
- protozoa, direct lifecycle
- obligate
- flagella (movement) + adhesive disk
- 8 species: A and B are infectious for humans
- cause diarrheal disease: giardiasis, GI mucosa infection
Transmission: Fecal-oral transmission, direct (human-human), indirect(cont.pr-human), zoonosis (domestic pets). Can contaminate soil, surfaces, food and fluids via faeces
Appears to be seasonal (august)
Cysts: can survive outside the body (soil, water -> months)
Ingestion of cysts, in the small intestines the cysts releases two trophozoites (excystation). The trophozoites multiply via binary fission (asexual). The trophozoites move towards the colon where they transform back into a cyst (encystation). The cysts gets excreted via faeces again.
Diagnosis:
- Triple-faeces-test (TFT): presence of cysts in faeces, three days samples, as cysts are not always present
- ELISA; presence of antigens in faeces
- Biopsy of small intestine via gastroscopy (strong suspicion for infection, but the other methods are negative)
- PCR; RT and multiplex
Pathogenesis and clinical symptoms:
- asymptomatic (50-75% cases)
- symptoms in small children and immune-compromised individuals
- diarrheal symptoms, gas, nausea, abdominal cramps
- chronic symptoms: weight loss, malaise, fatigue
Giardia:
Giardiasis Intestinal Asymptomatic Rivers Diarrhae Infectious Asexual
Toxoplasma gondii
- obligate intracellular protozoan
- infects warm-blooded vertebrates
- indirect life cycle
- definitive host: felids
Unsporulated oocysts are shed in the cat’s feces. The oocysts sporulate in the environment and become infective. The oocysts can persist in the environment for months. The human intermediate host become infected after ingesting contaminated food, water, blood transfusion or transplacentally from mother to fetus. In the host, oocysts transform into tachyzoites (motile and replicative, stimulated by proteases and acids) which localize in neural and muscle tissue (invade intestinal epithelial cells: parasitophorus vacuole). Cells burst and release tachyzoites into bloodstream and spread though the body (clinical symptoms). The tachyzoites localize in tissue and develop into tissue cyst bradyzoites (slow replicative); most commonly in skeletal muscle, myocardium, brain and eyes and may remain throughout the life of the host. Felids are then infected via ingestion of bradyzoites > merizoites
Symptoms:
- immunocompetent: asymptomatic, 10-20% flu-like symptoms due to immune response. Cysts are not immune reactive (phenotype switch tachyzoites to bradyzoites stimulated by immune pressure). Immuno compromised and young children (no phenotype switch): tachyzoites enter CNS and are able to form necrotic abscesses: damage.
Bradyzoites can differentiate back to trachyzoites when the hosts gets immunosuppressed
- encephalitits, myocarditis
- humans: accidental and (mostly) dead-end host
Diagnosis:
- serology: IgG and IgM antibodies (double+: early infection, G+/M-:late infection, G-/M+: negative)
- cysts may observed via tissue biopsy (invasive)
Dientameoeba fragilis
protozoan flagellate
- Transmission still under investigation, direct lifecycle?
Assumption: trophozoites present in the lumen of the large intestines where they multiply via binary fission and are shed into the feces. Rare putative cysts and precysts forms have been described in human clinical specimens; whether and in what settings transmission to humans occurs via ingestion of such forms is not yet known. Transmission via helminth eggs (Enterobius vermicularis/pinworm) has been postulated.
- trophozoites transmission: fecal-oral
- trophozoites fragile: not survive outside host
- primarily parasite of humans, trophozoites have been identified in other mammals (non-primates, swines)
- symptoms: asymptomatic or nonspecific gastrointestinal symptoms (colitis, appendicitis, irritable bowel syndrome)
Diagnosis: stain of trophozoites in fecal samples (microscopy), PCR
Ascaris lumbricoides
- metazoan: nematodes (roundworms)
- soil transmitted helminths (direct lifecycle)
- females: 20-35cm, males: 15-30 cm
Adult worms reside in the lumen of the small intestines. The female may produce ±200,000 eggs/day which are secreted via feces. Within the fertilized eggs (human is definitive host), larvae develop (18d-weeks). The unfertilized eggs will not develop further and are not infective. After ingestion of a fertilized egg, the larvae hatch in the intestine and invade the intestinal mucosa to the blood circulation. Here, they are carried to the lungs. In the lungs the larvae mature (10-14d) and penetrate the alveolar walls, ascend to the throat and are swallowed. In the small intestine, they develop into adult worms. Egg production by female worms occurs 2-3 month post ingestion. The adult worm can live 1-2years.
Symptoms: no acute symptoms. High worm burdens may cause abdominal pain and intestinal obstruction and malnutrition, risk for perforation in high intensity infections. Migrating adult worms may cause symptomatic occlusion of the biliary tract, appendicitis, nasopharyngeal expulsions
Diagnosis:
- microscopy: eggs in faeces (fixate sample)
- larvae can be idenitified in sputim during pulmonary migration phase
- adult worms occasionally present in stool or through mouth/nose (macroscopically recognizable)
