Lecture 6: Parasitology II

Vector borne

diseases transmitted by living organisms, called vectors, like mosquitoes, ticks, and flies, which spread pathogens from one host to another

Epimastigote location and function

a motile stage in the life cycle of some protozoan parasites by a flagellum that extends from the anterior of the cell and is attached to the body for part of its length by an undulating membrane found posteriorly host insect midgut and is dividing form

Metacyclic trypomastigote location and function

found in insects gut/feces and is the infective stage of the parasite, the form that’s released from the insect vector

Amastigote location and function

a non-motile, ovoid parasitic cell that is the intracellular stage in the life cycle of certain protozoa and found in human cells and intracellularly divide

Trypomastigote location and function

a motile, flagella posteriorly w/ undulating membrane, parasitic protozoan that is the form of the parasite found in the blood of an infected host and found in human bloodstream and circulate and infects bugs

Kinetoplastid protozoa

group of flagellated microorganisms that are distinguished by a unique organelle called a kinetoplast

kinetoplast

mass of mitochondrial DNA located at the base of their flagellum

Kinetoplastid Protozoa species

Leishmania, Trypanosoma cruzi, and Trypanosoma brucei

Leishmaniasis

organism leishmania and is found in blood and tissues

Leishmaniasis 3 main forms 

Cutaneous, mucocutaneous, and visceral

Leishmaniasis Cutaneous

causes skin sores that can develop into ulcers and abundant amastigotes in lesions

Leishmaniasis Cutaneous Treatment

spontaneous healing; strain-specific immunity; scarring

Leishmaniasis mucocutaneous

starts out like cutaneous more severe form that can cause destructive lesions in the nose, mouth, and throat, amastigotes in lesions

Leishmaniasis mucocutaneous Treatment

chemotherapeutic cure leads to immunity or antimonials but not always effective

Leishmaniasis visceral

the most serious, affecting internal organs and potentially causing death if untreated, with symptoms like fever, weight loss, and an enlarged spleen and liver

Leishmaniasis visceral Treatment

chemotherapeutic cure leads to immunity or miltefosine (drug)

Leishmaniasis reservoir and transmission

Domestic and wild animals like dogs and rodents, spread by vector borne sandfly

Leishmaniasis Epidemiology

tropical and subtropical regions and middle east b/c contact with sandfly and reservoir habitat

Leishmania: Promastigote

The flagellated (single anterior flagella), motile stage of Leishmania found in the sandfly vector, this is the infective form that lives extracellularly in sandfly’s gut

Leishmania: Amastigote

The non-flagellated, intracellular stage of Leishmania found in hosts, it resides and multiplies inside macrophages

Proboscis

elongated, tubular mouthpart of the sandfly (or other insects) used for piercing the skin and sucking fluids, this is used to inject promastigotes in human skin

Leishmania Life Cycle

1.Sandfly bites → injects promastigotes (motile) into human.

2.Promastigotes → enter macrophages → become amastigotes (non motile).

3.Amastigotes multiply → infect new cells → cause disease.

4.Sandfly bites infected human → ingests amastigotes

Leishmania Life Cycle summary

In sandfly: amastigotes → promastigotes → migrate to proboscis 

Cycle repeats

Leishmania diagnosis

amastigotes in needle biopsies or aspirates

African Trypanosomiasis location and transmission

Blood, lymphatic, and tissues and spread by vector bornes Tsetse fly

African Trypanosomiasis epidemiology

exclusively sub-Saharan; endemic in tsetse habitat

African Trypanosomiasis prevention

vector avoidance, vector control and monitor susceptible population, aggressive treatment

Trypanosoma brucei is a 

the protozoan parasite that causes African trypanosomiasis (African sleeping sickness)

Trypanosoma brucei alternates b/t 2 hosts:

tsetse fly which is the vector and a mammalian host (including humans and animals)

Trypomastigotes

one of the main forms of Trypanosoma species and are flagellated (motile), elongated stage found in the bloodstream of hosts

Life Cycle of Trypanosoma brucei

Tsetse fly bites and injects metacyclic trypomastigotes → bloodstream infection → slender forms multiply → stumpy forms ingested by new fly and transform in midgut → mature in salivary glands and infect next mammal.

Life Cycle of Trypanosoma brucei: Long slender

host is mammals, dividing trypomastigote and causes infection and evades immune system

This shape allows the parasite to express VSG - antigen variation

Life Cycle of Trypanosoma brucei: Short stumpy

host is mammal, non dividing trypomastigote, and is infective to tsetse fly

too small to divide, specifically infect tsetse fly not humans, job is to transmission - stress resistant

Life Cycle of Trypanosoma brucei: Procyclic

Host is fly midgut (only!!), job is dividing trypomastigote, and is adapted to fly environment

Life Cycle of Trypanosoma brucei: Metacyclic

Host is fly salivary glands, Infective trypomastigote, and is then transmitted to mammal

-non dividing, job is to infect humans

Why does African Trypanosomiasis need 2 hosts ?

the parasite needs a mammal (human or animals) to multiply and a tsetse fly to complete its life cycle

African Trypanosomiasis Immunity

initial humoral response to immunosuppression but then immune evasion by antigenic variation

African Trypanosomiasis Diagnosis

direct examination of blood, lymph, and CSF and card agglutination test, T. gambiense only

African Trypanosomiasis Treatment

if infection is early simple drugs are good, if infection is late the drug needs to cross blood brain barrier

Antigenic variation in Trypanosoma brucei (African)

covers its surface with a dense coat of variant Surface Glycoprotein (VSG), its able to constantly switches which VSG gene it expresses antigen evading the immune system

-happens only in slender form

Winterbottom’s Sign

swelling of lymph nodes in the back of the neck, a key early symptom of African trypanosomiasis (sleeping sickness) caused by the parasite Trypanosoma brucei

South American Trypanosomiasis (AKA chaga’s disease)

Caused by Trypanosoma cruzi and reservoir are rats, cats, dogs, and opossum

South American Trypanosomiasis location and transmission

Found in blood, lymphatics & tissues and spread by vector borne reduvid bugs

South American Trypanosomiasis Prevention

vector control; good housing; screen blood supply

Life Cycle of Trypanosoma cruzi

alternates between insects and humans (2 hosts), using amastigote and trypomastigote forms to multiply and spread. Infection occurs when infective feces of the reduvid bug contaminate a bite wound, leading to Chagas disease

Life Cycle of Trypanosoma cruzi specific

Metacyclic trypomastigote: delivered in bug feces that invades human cells

Amastigote: inside host cells, no flagella, and major dividing stage in humans

Bloodstream trypomastigote: non-dividing form in blood and ingested by reduvid bug

Epimastigote: in insect midgut where it divides in bug and comes back into metacyclic trypomastigote

South American Trypanosomiasis Acute pathology

2-4 months fever, chagoma (Romana’s sign), hematogenous spread; circulating trypomastigotes

- severe in children;

South American Trypanosomiasis Chronic pathology

10-20 years no trypomastigotes but persistent amastigotes, tissue damage, and heart attack is common

South American Trypanosomiasis Diagnosis

acute: trypomastigotes in blood

chronic: serology, xenodiagnosis

schizogony

asexual reproduction by multiple fission, found in some protozoa, especially parasitic sporozoans

sporulation

in sexually reproducing parasites, sporulation can result from the fusion of gametes (formed from haploid gametophytes) to create a diploid zygote,

Apicomplexan Parasites Characteristics

Obligate intracellular parasites, apical intracellular organelle, and lifecycle is asexual and sexual (found in intestinal epithelial of host)

Toxoplasmosis

caused by organism Toxoplasma gondii and found in tissue/blood

Toxoplasmosis reservoir and prevention

cats, mice, sheep and prevented by avoidance behavior by at risk populations

Toxoplasmosis transmissions

spread ingestively: fecal/oral or undercooked meat

spread transplacental: congenital (birth) infection

Toxoplasmosis Epidemiology

world wide disease in developing countries for undercooked meat, hygiene, congenital, and cats

oocysts

environmental, infective stage of Toxoplasma gondii, it is a thick highly resistant structure that allows parasite to survive and spread infection

Cats

are the only definite host were toxoplasma can undergo sexual reproduction, only ones that produce oocysts

Toxoplasma gondii reproduces

sexually in cats (in intestine only) and asexually in other animals and humans, infection is spread via cat feces (oocytes) or undercooked meat

Toxoplasma gondii has 2 life cycles

Natural cycle: cats definite host

Incidental cycle: human incidental host

Rodents/birds: intermediate host

Toxoplasma life cycle: cats

Toxoplasma undergoes sexual reproduction in cats where the parasite multiples in the gut, cats shed immature oocysts in feces, then intermediate hosts rodents/birds ingest oocysts and parasites convert into tachyzoites which then form tissue cysts (bradyzoites)

Toxoplasma life cycle: humans

accidental hosts eat undercooked meat containing tissue cysts, parasites turn into tachyzoites that spread thru body, and the cycle ends here b/c these hosts cant shed oocysts

Two Phases of Toxoplasma Infection

Tachyzoite and Bradyzoite

Toxoplasma Tachyzoite

rapid replicative form during initial acute infection caused by reactivation of dormant cysts, and control by primary immune system

- can cross placenta, causes encephalitis in AIDS

Toxoplasma Bradyzoite

encysted slow growing form during dormant phase, source of reactivation throughout life-long infection, and control by memory immune response

Toxoplasmosis Diagnosis

 serology; indirect immunofluorescence (IFA) and seizure in AIDS: MRI, treat, repeat MRI

Toxoplasmosis Treatment

essential for immunocompromised or active chorioretinitis and prevented by breaking the transmission cycle