Parasitology Flashcards
the parasites causing malaria and mention malaria types
Plasmodium vivax Benign tertian malaria
Plasmodium ovale Ovale tertian malaria
Plasmodium malariae Quartan malaria
Plasmodium falciparum Malignant tertian malaria
the mode of infection of Plasmodium
the anopheles injects the sporozoites into the blood
the infective stage of plasmodium
sporozoites
definitive host of plasmodium
female anopheles
hypnozoite are related to
liver phase of P.vivax and P. ovale
the cycle of the malaria disease (plasmodium)
do check it
Rupture of infected red blood cell of plasmodium occurs every
3rd day in P. vivax & P.ovale
4th day in P.malarie
irreg. in P.falciprum
diagnostic stages of Plasmodium
schizont, late trophozoite, early trophozoite (ring form), gametocytes
pathogenesis of malaria
- Malaria paroxysms
- haemolytic anemia
- hepatosplenomegaly
what is the stages of the malaria paroxysms (fever)
- Cold stage
The patient has sudden chill, extreme cold and his temperature rises(15minutes) - Hot stage
The patient has headache, high fever and hot, dry and flushed skin - Sweating stage
The patient has profuse sweating and temperature falls
why clinical attacks reappear after disappearing?
- due to Presence of hypnozoites in the liver[Relapse] which occurs in P. vivax and P. ovale
- Presence of low-grade parasitaemia when the patient becomes
immunosuppressed [Recrudescence] which occurs in P.malariae and P. falciparum
ages of RBCs that affect and its specific plasmodium
- Plasmodium vivax & Plasmodium ovale prefer to invade young RBCs
- Plasmodium malariae prefers toinvade old RBCs
- Plasmodium falciparum invades RBCs of any age
causes nephrotic syndrome
Chronic Plasmodium malariae infection due to deposition of immune complexes on glomerular wall to activate complement cascade leading to kidney tissue damage
complication of chronic P.malariae infection
Nephrotic syndrome
Complication of P.falciparum
- Knob formation on the infected RBCs which adhere to the blood capillaries so decrease blood supply so death of organ tissue
- Hyper-reactive malarial splenomegaly (Tropical splenomegaly syndrome)
- Black water fever
Lab diagnosis of Malaria
- Giemsa-stained thin & thick blood film examination to demonstrate the parasite stages
malaria pigments is a remnant of haemoglobin
Stippling: degeneration process occurring in Plasmodium infected RBCs
* Schuffner’s dots of vivax and ovale
* Ziemann’s dots of malariae
* Maurer’s clefts of falciparum
2- Detection of circulating parasite antigen using monoclonal antibodies
3- Detection of parasite DNA and RNA in patient’s blood using PCR
Tissue schizonticides of plasmodium
pyrimethamine or primaquine
Blood schizonticides of plasmodium
chloroquine or mefloquine
Blood gametocytes of plasmodium
chloroquine or primaquine
People that are naturally resistant to malaria infection
- Absence of Duffy antigen
- Haemoglobin S (in sickle-cell disease)
- Deficiency of G6PD enzyme
causes Microcytic Hypochromic anemia
Ancylostoma duodenale
trichuris Trichura
causes rectal prolapse
T. Trichura
causes macrocytic hyperchromic anemia
Diphyllobothrium Latum
2 morphological forms of Leishmania
amastigote intracellulary & promastigote in vector and in culture
species of visceral leishmania
- L. Donovani
- L. Infantum
- L. Chagasi
Morphology of Amastigote
Vesicular nucleus with large central karyosome
Kinetoplast (= origin of flagellum)
Morphology of promastigote
amastigote + free anterior flagellum
man is final host in?
leishmania
infectives stage of leishmania
promastigote injected by sandfly
diagnostic stage of leishmania
amastigote
intermadiate host of leishmania
sandfly
phlebotomus in old world
Lutzomyia in new world
mode of transmission of leishmania
1.Bite of female sand fly inoculating metacyclic promastigote.
2. Blood transfusion
3. Organ transplantation
4. Congenital
5. Accidental in lab worker
reservoir host
rats and rodents
Pathogenesis of leishmania
▪ Papule at site of bite (leishmanioma).
▪ Intermittent fever (double daily rise).
▪ L.N: Lymphadenopathy.
▪ Liver: hepatomegaly, pain and tenderness. reversal of albumin /globulin ratio. Why??????
▪ Spleen: splenomegaly & hypersplenism.
▪ Bone marrow: pancytopenia.
▪ Intestine: diarrhea with dysenteric manifestation d2 ulcers.
▪ Weight loss, cachexia, ascites.
▪ Kidney: renal failure d2 immune complex deposition.
▪ Decrease immunity: 2ry bacterial infections.
▪ Skin manifestations :
a) Dark pigmented erythematous areas (black fever)
b) PKDL(post-kala-azar dermal leishmaniasis) (d2 inadequate treatment).
RES KIIS
name of skin test on leismania
Motengro (Leishmanin)
results of Motengro (Leishmanin) skin Test:
-ve in active infection
+ve after 2 months of ttt.
Habitat of wuchereria bancrofti
the adults lives in lymph vessels and lymph
glands of man
definitive host of wuchereria bancrofti
man
vector (intermediate host) of Wuchereria Bancrofti
female culex mosquito
life cycle of Wuchereria Bancrofti
- Microfilariae laid by female worm which have smooth body curves, loose sheath and tail end free of nuclei go to lymph vessels then to general circulation through the wall of lymphatics or thoracic duct
- Microfilariae appear in peripheal blood at night between 10PM-2AM and disappear by day time(nocturnal periodicity)
- Female Culex mosquito sucks blood containing microfilariae
- In the stomach of the mosquito microfilariae lose their sheath and penetrate gut wall to the thoracic muscles
- They moult twice and on 10th day they become infective filariform larvae(1500x20u)then they migrate to the head and labium of the mosquito
- No multiplication of the larvae in the vector only growth(one microfilariaone infective filariform larvae)i.e Cyclodevelopmental transmission
- Cycle in the mosquito requires 2-3 weeks
p. 9 lect 5
causes of nocturnal periodicity of wuchereria Bancrofti
- Adaption
- Positive chemotaxis
- Decreased oxygen and increased carbon dioxide
- Khalils theory:reversal of sleeping hours is followed by reversal of periodicty (effect of gravity)
Pathogenesis of Wuchereria Bancrofti
- Acute inflammatory phase: due to immunological reactions to toxic
metabolites of adult worms and secondary bacterial infection usually by sterptococci - lymphangitis and lymphadenitis
- Chronic obstructive phase: fibrosis leads to obstrcution of lymphatic vessels leads to leakage of lymph under the skin with high protein content causing proliferation of c.t under the skin
- non pitting edema
- Elephantiasis: leg,scrotum,vulva(dependent sites)are usually affected
causes elephantiasis
Wuchereria Bancrofti
results of ruptered distended lymphatics
- Chylothorax(in pleural sac)
- Chylous ascites(in peritoneal sac)
- Chylocele(in tunica vaginalis of testes)
- Chylous diarrhoea(in intestine)
- Chyluria(in urinary tract)with passage of microfilariae in urine.
diagnosis of wuchereria bancrofti
Detection of microfilariae in blood they are highest at night(10pmto2am)in capillary blood(finger and ear lobe)
Diethylcarbamazine provocative test: microfilariae can be demonsterated at any time of the day
Concentration of microfilariae(knotts technique)
Detection of microfilariae in chylous urine
Detection of adults:ultrasonography,biopsy,lymphangiography
ELISA
EOSINOPHILIA.
TREATMENT of Wuchereria Bancrofti
- Diethylcarbamazine(DEC):lethal to microfilariae,antihistaminics,corticosteroids must
be added to prevent allergic reactions due to rapid
destruction of microfilariae . - Ivermectin; kill microfilariae repeated doses can kill adults.
- Antibiotics.
- Surgical treatment.
what is Occult filariasis
It is a syndrome characterized by:
* High eosinophilia
* High titre of antifilarial abs&IgE levels
* Paroxysmal cough(dry)
* Lymphadenopathy
* Low grade fever&wt loss
* The response to DEC is excellent
reservoirs of Brugia Malayi
Monkeys&Cats
its vector is mansonia
Brugia Malayi
vector of Brugia Malayi
Mansonia
ChronicPlasmodium malariaeinfection is complicated by
Nephrotic syndrome
ChronicPlasmodium malariaeinfection is complicated by
Nephrotic syndrome
complication of malignant malaria on affected organs
➢ The brain (cerebral malaria) drowsiness, convulsions & coma
➢ The lungs Lung oedema, difficulty in breathing
➢ The liver impaired glycogenolysis Hypoglycaemia
➢ The kidney Acute renal failure
➢ The intestine diarrhoea, dysentery
➢ Circulation (Algid Malaria) hypotension, circulatory collapse & shock
causes algid malaria
p. falciparum
what is algid malaria
hypotension,
circulatory collapse
shock
cause of the splenomegaly resulted from malignant malaria
due to the exaggerated immune response to repeated attacks of malaria so the spleen is marked by increased IgM production
clinical picture of black water fever caused by
fever and anemia
jaundice
hemoglobinuria
people resistant to p. vivax
peolpe that dont has duffy antigen
people that resistant to P. falciparum
Hemoglobin S people has sickle cell disease
Def of G6PD enzyme
Radical treatment after clinical attack of malaria
Primaquine
treatment during attack of malaria
Chloroquine
Chemoprophylaxis of malaria before entering endemic areas
pyrimethamine
primaquine
Chemoprophylaxis of malaria after entering endemic areas
Chloroquine
mefloquine
Other name of loa loa
African eye worm
Habitat of Loa Loa
Subcutaneous tissue
Has a diurnal periodicity
Micrrofilaria of Loa loa
The vector (intermediate host) of Loa Loa
Chrysops
Where is conversion of microfilaria to infected filariform Larvae
Thoracic muscles of chrysops fly
Type of transmission and development of Loa Loa in chrysops
Cyclodevelopmental
Clinical picture of Loa Loa infection
- Acute inflammatory reactions in the form of itching, creeping sensation, redness, oedema, burning pain.
- Granuloma in chronic stage (according to organ affected)
- Eye : oedema of the eye lids,pain,redness impaired vision the adult worm may be seen under conjunctiva
Associated with calabar swelling
Loa Loa
What is calabar swelling
allergic reaction caused by Loa Loa to worm metabolites
appears as localized hard non pitting subcutaneous
swelling on hands, wrists, elbows and ankle
Complication of Loa Loa infection
Invasion of the worm to ectopic foci causing orchitis, hydrocele, arthritis, glomerulonephritis
retinopathy, encephalopathy
Diagnosis of Loa Loa
- Clinical: eye worm and calabar swellings
- Laboratory: detection of microfilaria in blood in day time(10am-2pm)
- Serologic tests e.g ELISA
- Eosinophilia
Habitat of Onchocera volvulus
Subcutaneous nodules with fibrous tissue capsule
The vector transmitting onchocera volvulus
Simulium
Onchocera volvulus microfilaria migrate to
Surrounding skin
Location of onchocera nodules
bony prominances as scalp, elbow, knee, ribs iliac crests and scapula
Cause river blindness
Onchocera volvulus
Cause sudan blindness
Onchocera volvulus
Clinical picture of onchocera volvulus
Onchocera nodules
Eye lesion (River blindness)
Migration of microdfilaria leads to keratitis,retinitis,chorioditis and optic neuritis with
subsequent fibrosis leads to blindness
Dermatitis:itching and oedema in early stage then
fibrosis in late cases leads to skin atrophy and loss of skin elasticity with wrinkling(premature senility) and hanging groin
* Depigmentation : in black people (leopard skin) or
hyperpigmentation in Yemem(Sowda)
Causes blepharospasm
Onchocera volvulus
Early ocular symptoms of onchocera volvulus
- Photophobia, Lacrimation
- Blepherospasm
- F.B sensation
Causes leopard skin
Onchocera volvulus
Complications of onchocera volvulus
- Lymphadenitis: regional lymph nodes may be
enlarged(immune reaction) - Elephantiasis :mainly of external genitalia is seen in some parts of Africa
- Arthropathy:due to immune complexes
- Encephalitis and epilepsy:microfilaria may erode skull
Diagnosis of onchocera volvulus
- Aspirate of the nodules or bloodless skin snip reveals
microfilariae - Biopsy of the nodules reveals Adults.
- Eosinophilia
- Mazzotti test:
- Patch test
What mazzoti test
Oral dose of diethylcarbamazine(DEC)
provoke intense pruritis with in a few hours due to
death of microfilaria
What is patch test
Oral dose of 50mg diethylcarbamazine(DEC)
provoke intense pruritis with in a few hours due to
death of microfilaria
mazzoti test is used for
diagnosis of onchocera volvulus
What are parasites causing anemia
Ancylostoma duodenale, Trichuris trichura, Diphyllobothrium latum
Life cycle of ancylostoma duodenale
Adults in S.i»> Immature eggs in stool moist
warm soil (1-2d)»> hatching & release 1st stage
rhabditiform larva moulting twice within
one week (infective filariform larva )»>
penetrate the skin venules or lymphatics»>
heart lungs (3rd moult) penetrate the
pulmonary capillaries to alveoli migrate up
through the trachea swallowed»> small
intestine 4th moult(adult)
Causes Loeffler’s syndrome
ancylostoma duodenale
What is Loeffler’s syndrome
verminous pneumonitis, fever, cough, dyspnea, minute hemorrhage, hemoptysis & eosinophilia
Clinical picture of ancylostoma duodenale
1)Skin lesions:
ground itch or hookworm dermatitis.
2)Pulmonary lesion: (Loeffler’s syndrome)
verminous pneumonitis, fever, cough, dyspnea, minute hemorrhage, hemoptysis & eosinophilia a
3) Intestinal lesion: hemorrhage due to sucking and producing anticoagulants and attachment of different sites of mucos
Microcytic Hypochromic anemia due to chronic
blood loss & depletion of iron stores
- Subcutaneous edema due to hypo-proteinemia
- Melena & occult blood in stool may occur.
- Gastrointestinal symptoms:
nausea, vomiting, abdominal pain
5)Pica :
habitual ingestion of non-food substances as soil.
6) physical and mental Retardation
Laboratory diagnosis of ancylostomata duodenale
- Stool examination for eggs
- Occult blood in stool
- Microcytic hypochromic anemia & eosinophilia
Treatment of ancylostoma duodenale
1- Albendazole
2- Mebendazole
3-Iron supplementation
4- protein rich diet.
Life cycle of trichuris trichura
Adults in caecum immature eggs in faeces
soil 10-21d» embryonated egg (Rhabditiform larvae)» ingestion» hatching in lower part of S.I.»_space;larva» Temporary growth of the larva(1 w)» larva pass to the caecum»_space;Larva attach to mucosa of caecum maturation adult
Mode of infection ancylostoma duodenale
Filariform larva
Mode of infection of Trichuris trichura
ingestion of contaminated water, green vegetable
containg embryonated egg or via soil contaminated
hands
Clinical picture of Trichuris Trichura
b) Dysentery & tenesmus.
c) Chronic blood loss (0.005 ml/ worm/d)due to
oozing from site of worm attachment to
mucosa leading to anemia, nutritional
deficiency & weight loss
d) Anemia: due to
-bleeding microcytic hypochromic anemia.
-Toxic products of the worm macrocytic
hyperchromic anemia (Trichocephalic anemia).
e) moderate eosinophillia
f) Rectal prolapse.
g) Rarely perforation: lead to peritonitis.
h) appendicitis
Laboratory diagnosis of Trichuris Trichura
a. Stool examination for egg detection.
b- Rectal examination by proctoscopy: in heavy
infection
hyperemic edematous mucosa with hanging worms
from the mucosa.
c- Barium enema: may show translucent adult.
d- cbc:
- Moderate eosinophilia
- Anemia
Mode of infection of Diphyllobothrium latum
ingestion of improperly cooked fish (fresh water fish
e.g. salmon) containing plerocercoid larva
Treatment of Diphyllobothrium latum
1-Praziquantel
2-Niclosamide followed by saline purge.
3-Vit. B12 supplementation.
Clinical picture of Diphyllobothrium latum
- Hunger pain, weight loss, vomiting, diarrhea
- Pernicious anemia (megaloplastic) due to toxins and B12 def
- Neurological manifestation as convulsions and insomnia
- Intestinal obstruction due to large number of the worm
- Migrating segment can cause cholecystitis and cholangitis
Cause cholecystitis
Cause cholangitis
Migrating segments of Diphyllobothrium latum
Migrating segments of Diphyllobothrium latum
Causes B12 def
Diphyllobothrium latum
Causes melena
Ancylostoma
Clinical picture of early intrauterine infection 1st trimester of toxoplasma
Spontaneous abortion
Retinochoroiditis
Encephalomyelitis
Clinical picture of Late intrauterine infection 3rd trimester of toxoplasma
Still birth
Retinochoroiditis due to calcification
Encephalitis due to calcification
Clinical picture of neonatal infection of toxoplasma
Pneumonitis
Hepatosplenomegaly
Jaundice
Convulsions
Mental retardation
blindness
Clincal picture of infection of toxoplasma among immunocomptent
Myalgia,extreme fatigue with generalized
lymphadenopathy which mimics infectious
mononucleosis
Clinical picture of Infection of toxoplasma among immunocopromized
CNS infection» ataxia, convulsions and hemiparesis, with increase antitoxoplasma IgG
Habitat of leishmania parasites
Reticuloendothelial cells and organs
LN, bone marrow, liver, spleen
Visceral leishmania in old world
- L. Donovani
2.L. Infantum
Visceral leishmania in new world
L. Chagasi
2 morphological forms of leishmania
amastigote intracellulary &
promastigote in vector and in culture
Final host, infective, diagnostic, I.H, R.H of leishmania
Man,
promastigote,
amastigote,
sandfly (phlebotmus in old and lutzonia in new)
dogs and rodents
Mode of transmission of leishmania
1.Bite of female sand fly inoculating metacyclic promastigote.
2. Blood transfusion
3. Organ transplantation
4. Congenital
5. Accidental in lab worker
We culture in NNN media to diagnose
Promastigote of leishmania
Diagnose of leishmania
*microscopic examination of samples (blood,
liver, L.N, spleen) and stain with giemsa stain.
*Culture on NNN media (promastigote)
*Animal inoculation (amastigote)
*PCR
We use motengro test in diagnosis of
Leishmania
-ve in active infection,
+ve after 2 months of ttt.
