The family of trypanosomatidae contains only two genera that parasitize humans:
Genus Trypanosoma found either in circulating blood or intracellularly (in cardiac muscle) in African blood; American Blood and cardiac muscle
Genus Leishmania always intracellular, principally in the cell of the reticulo-endothelial system
Hemoflagellates have up to eight life cycle stages which differ in the placement and origin of the flagellum:
Two stages may occur in vertebrate hosts: the amastigote and the trypomastigote
Three stages may occur in invertebrate hosts: the promastigote, paramastigote, and epimastigote
A trypanosomatic cell has the kinetoplast, a unique organelle rich in DNA (kDNA)
Two types of DNA molecules are found in kinetoplast: maxicircles which encode important mitochondrial enzymes, and minicircles which function in RNA editing
The kinetoplast is reddish purple in Giemsa stain and darker than the nucleus, contrasting with the pale blue cytoplasm
American Trypanosomiasis (Chagas Disease):
First described by Carlos Chagas in 1911
Leading cause of non-ischemic congestive heart failure worldwide, notably in Latin America where it is endemic
Life Cycle of Trypanosoma cruzi:
Transmitted by the Reduviid (Triatomine) bug
Infection leads to local inflammatory reaction, chagoma formation, and spread to various organs including the heart, skeletal muscles, and nervous system
Epidemiology of Chagas Disease:
Approximately 16-18 million people are infected worldwide
Disease is limited to the Western Hemisphere, prevalent in Mexico, Central America, and South America
Morbidity/mortality: acute phase mortality is 5%, with over 70,000 annual deaths; leading cause of congestive heart failure in Latin America
Clinical Presentation of Chagas Disease:
Early phase is typically asymptomatic
Acute phase symptoms include flu-like illness with high temperature, chills, headache, irritability, tiredness, and more
Symptoms of Chagas disease include a flulike illness with high temperature, chills, headache, irritability, tiredness, anorexia, malaise, myalgias, lymphadenopathy, and splenomegaly
In chronic Chagas disease, the gastrointestinal system may be involved, leading to symptoms like dysphagia, regurgitation, hiccups, constipation, and abdominal pain
Patients with colon affectation in Chagas disease may experience slow progressive constipation, with most patients with megacolon having a bowel movement every 10 days
Clinical presentation of Chagas disease may include Romaña sign (if the bite is close to the eye), hepatosplenomegaly, meningoencephalitis more common in young infants, and cardiovascular abnormalities like cardiac enlargement, functional murmurs, and conduction blocks
Laboratory studies for Chagas disease involve blood film CBC count, serologic tests like complement fixation (CF), indirect immunofluorescence (IFAT), enzyme-linked immunosorbent assay (ELISA), polymerase chain reaction (PCR) to observe T. cruzi kinetoplast DNA, and Xenodiagnosis
Investigations for Chagas disease include chest radiography, electrocardiography (ECG), echocardiography, cardiac MRI, fluoroscopic esophagrams, manometry revealing loss of peristalsis, and barium enema examination as the cornerstone for diagnosis
Histologic findings in Chagas disease show lymphocytic, monocytic, and eosinophilic infiltration in the portal of entry lesion, and in the invaded heart, there is diffuse inflammation of the myocardium with dense foci of fibrosis and invasion of inflammatory cells
Management of Chagas disease involves medical treatment with nifurtimox or benznidazole in the acute phase, surgical control by using insecticides to eliminate vector bugs from dwellings, improving the household environment, community participation strategies, and serologic screening in blood banks in endemic areas
African Trypanosomiasis, also known as Sleeping Sickness, is caused by the flagellate protozoan Trypanosoma brucei, with two subspecies: T. b. rhodesiense (East African) and T. b. gambiense (West African)
African Trypanosomiasis is transmitted by the bite of infected tsetse flies during daylight hours, with vertical transmission to unborn babies, blood transfusion, or sexual contact
Tsetse flies, the vectors for African Trypanosomiasis, are large, biting flies that inhabit much of tropical Africa, and they are obligate parasites feeding on the blood of vertebrate animals
[An obligate parasite or holoparasite is a parasitic organism that cannot complete its life-cycle without exploiting a suitable host]
The life cycle of Trypanosoma brucei gambiense & T. b. rhodesiense involves transmission by tsetse flies and different stages of infection in humans
Epidemiology of African Trypanosomiasis shows it affects 36 countries in sub-Saharan Africa, with a decrease in prevalence since 2000, and during epidemic periods, prevalence can reach 50% in certain regions
Symptoms of African Trypanosomiasis include intermittent fevers, rash, lymphadenopathy, and variations in surface antigens allow the parasites to evadespecific immunity
Pathology and clinical picture of African Trypanosomiasis involve different stages like skin chancre, haematolymphatic stage with generalized lymphadenopathy and organ involvement, and central nervous system stage with meningoencephalitis
Symptoms of African Trypanosomiasis progress from painful skin chancre to intermittent fever, malaise, myalgia, arthralgias, lymphadenopathy, and facial edema in some cases
Symptoms of late or neurologic stage of African Trypanosomiasis include persistent headaches, daytime somnolence followed by nighttime insomnia, and behavioral changes
Symptoms of stage 2 (late or neurologic stage) of trypanosomiasis include:
Persistent headaches refractory to analgesics
Daytime somnolence followed by nighttime insomnia
Behavioral changes, mood swings, and depression
Loss of appetite, wasting syndrome, and weight loss
Seizures in children (rarely in adults)
Physical findings in stage 1 (early or hemolymphatic stage) of trypanosomiasis include:
Chancre at bite site
Skin lesions (trypanids) in light-skinned patients
Lymphadenopathy (axillary and inguinal more common in East African trypanosomiasis, cervical more common in West African form)
Fevers, tachycardia, edema, weight loss, and organomegaly, particularly splenomegaly in T. brucei gambiense
Physical findings in stage 2 (late or neurologic stage) of trypanosomiasis include:
CNS manifestations like irritability, tremors, increased muscle rigidity, occasional ataxia, and hemiparesis
Kerandel sign (delayed pain on compression of soft tissue,Severe, delayed pain when soft tissues are compressed)
Behavioral changes consistent with mania or psychosis, speech disorders, psychosis, sensory disorders, and seizures
Stupor and coma (giving rise to the name sleeping sickness)
Complications of late or neurologic stage of trypanosomiasis include:
Anemia and fatigue
Wasting syndrome
Aspiration pneumonia
Meningoencephalitis and seizures
Stupor or coma (sleeping sickness)
Perinatal death or abortion (after congenital infection), death
Investigations for trypanosomiasis:
Blood: anemia, hypergammaglobulinemia[is an uncommon condition characterized by elevated levels of immunoglobulins in your blood], elevated ESR, thrombocytopenia, hypoalbuminemia
Blood Smear: unstained blood smear or a Giemsa-stained thick smear (more sensitive) for mobile trypanosomes
CSF: high total IgM, high CSF protein level
Serology: card agglutination test for trypanosomiasis (CATT) for West African trypanosomiasis
Treatment for trypanosomiasis:
Melarsoprol for East African trypanosomiasis
Eflornithine for West African trypanosomiasis
Other drugs: Suramin, Pentamidine isethionate, Fexinidazole
Leishmaniasis is a parasitic infection caused by kinetoplastid protozoans in the genera Leishmania and Endotrypanum, transmitted through the bite of sand flies
Classification of Leishmaniasis:
Clinical disease: divided into 3 primary clinical forms - Cutaneous, Mucocutaneous, and Visceral
Geographic occurrence: Old World leishmaniasis (Africa, Asia, Middle East, Mediterranean, India) and New World leishmaniasis (Central and South America)
Cutaneous leishmaniasis,(CL) is the most common form and causes skin lesions, mainly ulcers, on exposed parts of the body, It includes:
Localized cutaneous leishmaniasis
Diffuse (disseminated) cutaneous leishmaniasis
Leishmaniasis recidivans : a prolonged, relapsing form ofcutaneous leishmaniasisresembling tuberculosis of the skin that may persist for many years with a chronic and relapsing course.
Post-kala-azar dermal leishmaniasis
Mucocutaneous leishmaniasis consists of the relentless destruction of the oropharynx and nose, resulting in extensive midfacial destruction, with optical and genital mucosal involvement in severe cases
Visceral leishmaniasis (kala-azar) is a potentially lethal widespread systemic disease characterized by darkening of the skin, fever, weight loss, hepatosplenomegaly, pancytopenia, and hypergammaglobulinemia
Diagnosis of Leishmaniasis includes:
Isolation, microscopy, and culturing of the parasite from infected tissue
Serologic detection of antibodies to recombinant K39 antigen
Medical: Pentavalent antimony, Liposomal amphotericin B (AmBisome), Intramuscular pentamidine, orally administered ketoconazole, itraconazole, fluconazole, allopurinol, and dapsone, topical paromomycin
Control of local infection
These protozoans require hematin obtained from blood hemoglobin for aerobic respiration, hence they are called hemoflagellates
the 5 stages out of 8. notice the flagellum and their postions
Romaña sign, also known as the periorbital swelling syndrome, refers to periorbital swelling, palpebral edema and conjunctivitis seen 1-2 weeks following infection with Trypanosoma cruzi (causative agent in Chagas disease). basically a swelling all around the eye