BABESIA SPECIES • ZOONOSIS • Vector-IXODID tick • Resorvoir host-mice,voles and other rodents • Babesia microti-common cause of babesiosis in US
Life cycle
• Infective stage-pyriform bodies • Diagnostic stage-trophozoite • In RBC-trophozoites by binary fission
forms tetrad-lyse erythrocytes-release merozoites-reinfect • Infected cells-ingested by tickstransovarian transmission
Clinical features • Incubation period-1-4 weeks • Malaise,fever,chills,headache,fatigue • No periodicity • Progresses to develop hemolytic anemia • Splenomegaly,hepatomegaly,renal failure
Lab diagnosis • Microscopic examination of blood
smears • Resemble the ring forms of Plasmodium species • But no pigment or other stages of growth as in plasmodium
Treatment and control • DOC-Clindamycin+quinine • Exchange blood transfusion in pts
who had splenenctomy and severe infections • Protective clothing,insect repellents
TOXOPLASMA GONDII • Coccidian parasite • Reservoir host-house cat • Infective stage-sporulated oocyst • Diagnostic stage-immature oocyst in feces
• Some trophozoite forms-crescentic
tachyzoites-responsible for initial infection • Slow growing shorter formsbradyzoites-cysts in chronic infection • More severe CNS disease in immunocompromised individuals
Clinical features • Mostly-benign and asymptomatic •-
headche,myalgia,fatigue,lymphadeniti s • c/clymphadenitis,rash,hepatitis,encephal opathy,myelitis,myocarditis,chorioreti nitis-blindness
• Congenital infection• 1st trimester-spontaneous
abortion,stillbirth • Afterwardsepilepsy,encephalitis,microcephaly,intr acranial calcifications,hydrocephalus,mental retardations,blindness,anemia,jaundice ,rash,pneumonia,diarrhoea
• In immunocompromised pts-
neurological • More than one lesion in the brain • Hemiparesis,seizures,visual impairment,confusioon,lethargy
Lab diagnosis • Serological testing-increasing
antibody titre • ELISA for IgM Ab • Demonstrating trophozoites and cysts in tissue and body fluids– defenitive method • Biopsy specimens
• Monoclonal antibody based staining • Culture methods
Treatment • Pyrimethamine+sulfadiazine high
dose,then continued in lower dose indefenitely • Trimethoprim-sulfamethoxazole is another option • Steroids-if cerebral oedema develops
• Prophylaxis-
sulfamethoxazole+trimethoprim • Avoid contact with undercooked meat
FREE LIVING AMOEBA • Naegleria • Acanthamoeba • Balamuthia • Common route-Inhalation of cysts
Clinical features • Naegleria fowleri- primary
meningoencephalitis • Frontal headache,sore throat,fever,blocked nose,positive Kernigs sign • Naegleria trophozoites - in brain on postmortem
• Acanthameoba and balamuthia-
granulomatous amoebic encephalitis and brain abscess in immunocompromised individuals • Acanthamoeba-keratitis(contact with contact lens,soil,dust) • Cutaneous infection
Lab Diagnosis • Specimens-Nasal
discharge,CSF,corneal scrapings • Saline wet preparation and iodine stained smears • Naegleria-only amoeboid trophozoite;other 2-cyst and trophozoite • Can be cultured on agar plates
Treatment, prevention and control • Naegleria-amphotercin B
+miconazole and rifampin • Acanthamoebapentamidine,ketoconazole,flucytosine • Balamuthiaclarithromycin,fluconazole,sulfadiazin e,flucytosine
• Amoebic keratitis-corneal
transplantation • Cutaneous infections-topical miconazole,chlorhexidine gluconate
LEISHMANIA • Hemoflagellate • Vector-sandfly-phlebotomus
• 3 speciesLeishmania donovani -visceral
leishmaniasis(kala-azar,dum dum fever) L.Tropica -cutaneous leishmaniasis(oriental sore,Delhi boil) L.braziliensis -mucocutaneous leishmaniasis(american leishmaniasis,espundia,chiclero ulcer)
Leishmania donovani
Sandfly Transmission • transmitted via mouthparts • promastigotes regurgitated from anterior gut • factors in saliva enhance infectivity
1) promastigotes 2) phagocytosis by macrophage → amastigote 3) replication within macrophage 4) release and phagocytosis of amastigotes
4) phagocytosis of amastigotes, or ingestion by vector 5) promastigotes • replication • attachment to epithelium
6) promastigotes
• Infective stage-promastigote • Diagnostic stage-amastigote • Resorvoir host-dogs,foxes,jackals
Clinical features • Gradual onset with fever,diarrhoea,
anemia • Progresses to enlargement of organs,weight loss • Post kala azar dermal leishmaniasis in persistent cases
Visceral Leishmaniasis • 3 possibly related species • L. donovani (Asia, Africa) • India (kala azar)
• reticuloendothelial system affected • spleen, liver, bone marrow, lymph nodes
• onset is generally insidious • progressive disease • 75-95% mortality if untreated • death generally within 2 years
Clinical Presentation • incubation period • generally 2-6 months • can range 10 days to years • fever, malaise, weakness • wasting despite good appetite • spleno- and hepatomegaly, enlarged lymph nodes • depressed hematopoiesis • severe anemia • leucopenia • thrombopenia → petechial hemorrhages in mucosa
Post Kala Azar Dermal Leishmaniasis • due to inadequate treatment • nodular lesions • easily cured with treatment (in contrast to DCL)
Lab diagnosis • Amastigote stage in tissue biopsy, bone marrow examination, lymph node aspiration • Serology • Culture of blood, bone marrow demonstrates the promastigote
Treatment • 1st drug of choice-oral miltefosine • Parenteral stibogluconate • Control of resorvoir hosts,protection from sandfly bite
L.tropica • Incubation period-2 weeks-2 months • 1 st sign –red papule at the site of bite • Intense itching-enlarges and ulcerates • Exudes a serous material-secondary bacterial infection
Cutaneous Leishmaniasis • incubation period: 2 weeks to several months • chronic ulcerated, papular, or nodular lesion • lesion is painless, nontender, non-pruritic and usually clean • occasionally satellite lesions and/or palpable lymph nodes
Diffuse Cutaneous Leishmaniasis • scaly, not ulcerated, nodules • chronic and painless • numerous parasites in lesions • seldom heal despite treatment L. mexicana
Lab diagnosis • Demonstration of amastigotes in stained smears • Serology • DNA probes
Treatment • DOC-stibogluconate • Application of heat to the lesion • Protection from bites
L.braziliensis • Clinical features similar to tropica • Involvement of mucus membranes and related tissue structures • Diagnosis and treatment-same as tropica
Mucocutaneous Leishmaniasis • primarily L. braziliensis (espudia) • two stages • simple skin lesion • 2o mucosal involvement • can occur long after primary lesion (up to 16 years) • frequently in nasopharyngeal mucosae • metastasis via blood or lymphatic systems • variable types and sizes of lesions • chronic and painless
TRYPANOSOMES • T.gambiense-african
trypanosomiasis(sleeping sickness) Vector-tsetse fly • T.cruzi-chagas disease(american trypanosomiasis) Vector-reduvids
T.gambiense
• Infective stage-metacyclic
trypomastigote • Diagnostic stage-blood stream trypomastigote
Clinical features • Earliest-an ulcer at the site of bite • Followed by
lymphadenopathy,fever,myalgia,arth ralgia • Posterior cervical lymphadenopathycharacteristic-WINTERBOTTOM SIGN • c/c-CNS involvement->death
• Winterbottom's sign is the swelling of
lymph nodes (lymphadenopathy) along the back of the neck, in the posterior cervical chain of lymph nodes, as trypanosomes travel in the lymphatic fluid and cause inflammation. • It may be suggestive of cerebral infection.
Lab diagnosis • Thick and thin blood films • aspirations from lymph node,
concentrated spinal fluid • Serology,immunoflurescence,ELISA,a gglutination methods
Treatment • -Suramin is the DOC • -melarsoprol is the DOC • Control breeding sites of the vector • Protective clothing
T.Cruzi
Clinical features • Earliest-development of a
chagoma(erythematous and indurated area) • Followed by a rash and edema around eyes and face • Fever, chills and rigor • CNS involvement
• c/c-
hepatosplenomegaly,myocarditis,enl argement of oesophagus and colon • Sudden death-heart block and brain damage
Lab diagnosis • Thick and thin films • Biopsy specimens from lymph nodes, liver spleen shows the Amastigote stage. • Serology • Xenodiagnosis • PCR
Treatment • DOC-NIFURTIMOX • Also allopurinol • Bug control, eradication of nests