PROTOZOAL DISEASES
In the bloodMalaria Trypanosomiasis
In the gutAmoebiasis Giardiasis
In the tissuesToxoplasmosis Leishmaniasis
AMOEBIASIS
It is caused by Entamoeba Histolytica which spread between humans by its cysts.PATHOGENESIS
Cysts of E. Histolytica are ingested in contaminated water and food. In the colon, vegetative trophozoite emerge from the cysts where they may invade the mucous membrane producing flask shaped ulcers.PATHOGENESIS
Localized granuloma (( AMOEBOMA)) is a rare complication amoebic ulcers may cause severe hemorrhage but rarely perforate the bowels.CLINICAL FEATURES
Incubation period from 2 weeks to many years Abdominal pain Diarrhea with mucous and blood & offensive odors
CLINICAL FEATURES
Tenderness over the line of the colon Diarrhea alternating with constipation is commonDIAGNOSIS
Clinical GSE: motile trophozoites containing RBCs Sigmoidoscopy: typical flask shaped ulcers, In endemic area one third of the population are symptomless( cyst passer )TREATMENT
Oral metronidizole 800 mg/8hr. for 5 days. OR Tinidazle 2 gm / day for 3 days Diloxanide furoate 500 mg /8 hr. for 10 days to eliminate luminal cysts.Amoebic Liver Abscess:
50% has no history of recent diarrhea Trophozoites may enter the portal venous radicale and carried to the liver causing an amoebic abscess.Amoebic Liver Abscess:
The liquid content at first pinkish colure which may later change to chocolate brown colure. Usually single and mainly in the right lobe.CLINICAL FEATURES
Asymptomatic, local discomfort, malaise, later swinging temperature and sweating but the patient not toxic. *Enlarged tender liver, cough, right shoulder pain.**Large abscess may penetrate the diaphragm and rupture into the lung or to the pleural cavity, peritoneal cavity or rarely to the pericardial sac.
DIAGNOSIS:
Clinical High WBC count predominantly neutophilia CXR shows elevated right dome of diaphragmDIAGNOSIS
Abdominal ultrasound Aspirated pus shows characteristic appearance and rarely amoeba Antibodies detected by IFAT in 95% of the cases.TREATMENT:
Early: metronidazole 800mg / 8hr. for 5 days or tinidazole 2 gm / day for 3 days. If the abscess is large or threaten to burst or if not responding to medical therapy, aspiration is requiredTREATMENT
Rupture to the pleura, peritoneal cavity or pericardial sac necessitates immediate aspiration or surgical drainage
GIARDIASIS
GIARDIASISIt is caused by Giardia Lamblia The cysts remain viable in water for up to 3 months and infection usually occur by ingestion of contaminated water. The flagellate attach to the mucosa of the duodenum and jejuenum.
CLINICAL FEATURES:
Incubation period 1 – 3 weeksDiarrhea, abdominal pain, weakness, anorexia, nausea and vomiting.CLINICAL FEATURES:
O/E there may be abdominal distention and tenderness Some patients run in chronic phase with lethargy, flatulence and loss of weight & malabsorption.
INVESTIGATIONS:
TREATMANT:Single dose of tinidazole 2 gm OR Metronidazole 2 gm once daily for 3 days OR Metronidazole 400mg/ 8 hr. for 10 days. OR Albendazole 400mg / day for 5 days.
MALARIA
MALARIAIt is caused by Plasmodium vivax, P. ovale, P. malariae and P. falciparum It is transmitted by the bite of female anopheline mosquitoes
LIFE CYCLE:
The female anopheline becomes infected when it feed on human blood containing gametocytes which develop in the mosquito over 1 – 3 weeks into sporozoitesLIFE CYCLE:
sporozoites which are transmitted to another persons via mosquito bites and then enter the liver to form merozoites which leave the liver and invade RBC where multiplication occursforming schizont which rupture to release more merozoites into the blood and causes fever. * The periodicity of the fever and rigor depend on the species of the parasite (( Tertian, Quartian, Aperiodic )) * P. vivax and P. ovale may persist in the liver as dormant
PATHOGENESIS:
The pathology of Malaria is due to hemolysis of the infected red cells and there adherence to capillaries. Anemia may developed and it worse by spleenomegaly P. Falciparum cause wide spread organ damage.CLINLCAL FEATURES:
P. vivax & P. ovale
Continuous fever for several days then classical boats of fever on alternated days (( cold phase and rigor for Ѕ - 1 hour, hot phase with flushing for several hours and gives a way to profuse sweating – wet phase- )) the cycle is repeated every 48 hr.P. vivax & P. ovale
Hepatospleenomegaly Anemia Herpes simplex is common Relapses are frequent in the first two years.P. Malariae
It is usually associated with mild symptoms boats of fever every third day it may cause GN and nephrotic syndromeP. Falciparum
insidious onset with malaise, headache and vomiting ( Flu – like ) cough and diarrhea are also common
P. Falciparum
The fever has no particular pattern Jaundice is common Hepatospleenomegaly and anemia developed rapidlyCerebral Malaria
Cerebral Malaria is a grave complication manifested by coma or confusion, no localizing sign and deathOther complication
Hypoglycemia pulmonary oedema acute renal failure severe anemia metabolic acidosis aspiration pneumonia shock
DIAGNOSIS:
Thick blood film for diagnosis to show the blood stage of the parasite. Thin blood film to identify the species of the parasite.TREATMENT:
P. vivax, P. ovale and P. malarae:Chloroquine 600 mg fallowed by 300 mg in 6 hours then 150 mg 12 hourly for 2 more days.
TREATMENTIn P. vivax and P. ovale, radical cure and prevention of relapses can be achieved with primaquine 15 mg daily for 14 days to destroy the hypnozoite phase in the liver.
P. falciparum:
Because of chloroquine resistance, Quinine is the drug of choice given 600 mg /8 hr. for 5 days fallowed by single dose of (( sulfadoxine 1.5 gm with pyrimethamin 75 mg )) 3 tab. Of fansidar.P. falciparum:
In pregnancy, 7days course of quinine should be given alone In quinine resistant area, Malarone , 4 tab. Once daily for 3 daysSevere malaria
Severe malaria is a medical emergency and cerebral malaria is the most common cause of death in malaria.Severe malaria
Quinine should be given i.v until the patient can take orally, active treatment of complication with fluid and electrolyte correction. Steroid has no role in treatment
PREVENTION:
1. Avoiding mosquito bitesLong sleeves and trousers should be worn Use of mosquito nets Repellent creams and sprays Impregnation of bed nets with permethrin.
2. Chemoprophylaxis:
Chloroquine sensitive area: Chloroquine 2 tab./ week & proguanil 1 tab. /day. Moderate Chloroquine resistant areas: Chloroquine 2 tab./ week & proguanil 2 tab. /day.PREVENTION:
High chloroquine resistant areas: Mefloquine I tab. Weekly or Doxycycline 100 mg daily or malarone 1 tab. Daily
3. Vaccination: still under trial.
TRYPANOSOMIASISAFRICAN TRYPANOSOMIASIS SLEEPING SICKNESS
It is caused by trypanosomes conveyed to human by bites of infected tsetse flies. Two types of trypansomes affect human in Africa:AFRICAN TRYPANOSOMIASIS
T. Brucei Gambianse: mainly at the riverside where the fly rests in the shade of trees and no animal reservoirs have been identified. T. Brucei Rhodesiense: it has a large reservoir in numerous wild animals
CLINICAL FEATURES:
A bite by the fly is painful and commonly inflamed and it again become painful and swollen about 10 days later (( Trypansomal chancre )) and the regional lymph node enlarge (( Winterbottom᾿s sign))CLINICAL FEATURES:
2 – 3 weeks later, it will invade the blood streamThe disease characterized by early heamatolympatic stage and late encephalitic stage.RHODESIENSE INFECTION:
The disease is more acute and severe and usually the patient is severely ill May developed pleural effusion, myocarditis or hepatitis. The patient may die before CNS involvement.GAMBIANSE INFECTION
Slow course over months or years with irregular boats of fever and enlarged lymph nodes mainly in the posterior triangle.
GAMBIANSE INFECTION
The spleen and the liver may become palpable CNS involvement after few months, headache, change in behavior, insomnia by night and sleepiness at day, confusion, coma and death.INVESTIGATIONS:
1. thin and thick blood film to demonstrate Trypanosome 2. puncture of the primary lesion and lymph node to demonstrate TrypanosomeINVESTIGATIONS:
3. serology by simple rapid card agglutination trypanosomal test (( CATT )).4. if CNS is affected, CSF will shows ↑ cells and protein and ↓ glucose.
TREATMENT
early treatment carry good prognosis for T. Rhodesiense: Suramin for T. Gambiense: Pentamidine for CNS involvement in both: MelarsoprolAMERICAN TRYPANSOMIASIS (( CHAGAS DISEASE ))
It is caused by T. cruzi transmitted to human from the faeces of the reduvidd bug Infected faeces are rubbed in through the conjunctiva, mucosa of the mouth or nose or skin abrasion.CLINICAL FEATURES
Acute phase:At the site of entrance, red, dusky firm swelling and enlargement of the regional lymph nodes Conjectival lesion cause unilateral firm reddish swelling of the lid may close the eye (( Romana᾿s sign ))
Acute phase
In few patients : skin rash, fever, lymphadenopathy and hepatospleenomegaly In few patients, acute myocarditis, heart failure or neurological features.Chronic phase:
Normal life span, asymptomatic, natural reservoir for the disease .After several years, 10 – 30 % develop low grade myocarditis and damage to the conducting fibers leading toChronic phase:
cardiomyopathy characterized by cardiac dilatation, arrhythmias, heart block and sudden death.In 10 % , damage to Auerbach᾿s plexsus result in dilatation of the alimentary tract mainly the oesophagus and colon so called (( Mega disease ))INVESTIGATIONS:
Blood film Serology
TREATMANT:Acute and early chronic (( 10 years )) : nifurtimox Cardiac or GIT : symptomatic, no specific treatment Mega disease: surgery may be useful.
LEISHMANIASIS:
It comprises several diverse clinical syndromes which can placed into 3 broad groups1. Visceral leishmaniasis (( Kala – azar )), caused by L. donovani2. cutaneous leishmaniasis caused by L. tropica and L. mexicana3. mucosal leishmaniasis caused by L.brasiliensis
it is zoonotic disease transmitted to human through phlebtomine sandfly vectors.
LIFE CYCLE:
Flagellar promastgotes are introduced by the feeding female sandfly and they taken by the human macrophage where they lose their flagellae and transform into amastigotes. These will multiply causes lysis of the microphage and infection of other cells.Sand fly pick up amastigote when feeding on infected patient or animal. In the sand fly, the parasite transform to flagellar promastigoites which multiply in the gut.
VISCERAL LEISHMANIASIS:Kala – azar
It is caused by L. donovani complexCLINICAL FEATURES:
it is predominantly a disease of childhood.Malnutrition and HIV infection increase the susceptibility to the visceral disease.Incubation period: weeks – months.
CLINICAL FEATURES:
At first high fever, rigor and chills then fever intensity will decrease and may present with double spike fever and afebrile in between.CLINICAL FEATURES:
Spleenomegaly developed quickly and become massive as the disease progresses and hepatomegaly occurs later. Lymphadenopathy may be seen ( generalized ).CLINICAL FEATURES:
Blackish discoloration of the skin is a feature of advanced illness and now seen rarely. Moderate to severe anemia that may lead to congestive heart failure.CLINICAL FEATURES
Bleeding tendency from retina, GIT and nose. Hypoalbuminemia lead to leg edema , ascites and anasarca.
CLINICAL FEATURES:
Immune suppression and secondary infectionare common and include TB, pneumonia, dysentery, herpes zoster, chicken pox, otitis media and skin infection. Without adequate treatment, most of the patients with clinical VL are likely to die.INVESTIGATIONS:
1. Pancytopenia with granulocytopenia and monocytosis 2. Hypergammaglobulinemia chiefly IgG. 3. HypoalbuminemiaDIAGNOSIS:
1. Demonstration of amastigotes ( Leishman – Donovan bodies ) in splenic smear is the most efficient mean of diagnosis but it carry a risk of serious hemorrhage.2. Bone marrow or lymph node smear are more save but less sensitive.
DIAGNOSIS:
3. PCR for DNA detection from the peripheral blood. 4. Serodiagnosis by ELISA or IFAT. 5. Direct agglutination test of stained promastigot. 6. Rapid immunochromographic strip test.DIFFRENTIAL DIAGNOSIS:
1.Malaria 2. Typhoid fever 3. Tuberculosis 4. Schistosomiasis 5. Blood diseases 6. LeukemiaTREATMENT:
1. Antimony compound ( Sb ): pentavalent antimony – Sodium stibogluconate – is the drug of choice at a dose of 20 mg / kg/ day given i.m or i.v for 28 – 30 days.S/E
arthralgia, myolgia, elevated liver enzymes, ECG will show T inversion, ST segment elevation, prolonged QT interval, ventricular ectopi, VT, VF and death.
TREATMENT:
2. Amphotericin B: 1mg/kg/day for 15 – 20 days used in Sb failure or resistance.S/E: renal,hepatic and cardiac toxicity.TREATMANT:
3. Miltifosine: oral drug, 100 mg/ day for 28 days but it is teratogenic drug.RESPONSE TO TREATMENT:
A good response result in abatement of fever,felling of well being, gradual decrease in splenic size, weight gain and recovery of the blood count.
RESPONSE TO TREATMENT:
Follow up for 6 – 12 months because some will relapse in form of enlargement of the spleen, return of fever,weight loss and decline in blood counts.Re- treatment with Sb or amphotericin B indicated.HIV – VL Co-infection
HIV increase the risk of contracting VL 100 – 1000 times.Atypical presentations are common, GIT involvement,HIV – VL Co-infection
Ascitis, plural effusion, pericardial effusion or oral mucosa involvement. Diagnosis and treatment are the same but relapses are common.POST- KALA – AZAR DERMAL LEISHMANIASIS (( PKDL ))
After treatment and recovery from VL, some patients develop dermatological manifestations seen as macules, papules, nodules and plaques especially at the area around the chin
PKDL
The diagnosis is clinical supported by slit skin smear to demonstrate the parasite or serological tests Treatment is difficult and may prolonged for 2 – 4 months.PREVENTION:
1. sand flies are extremely sensitive to insecticides and vector control through insecticides spray is very important.PREVENTION
2. use of mosquito net treated with insecticide. 3. early diagnosis and treatment of human infection.
CUTANEOUS LEISHMANIASIS
((oriental sore )) (( Baghdad boil ))causative agent
L. Tropica major L. Tropica minorCUTANEOUS LEISHMANIASIS
incubation period: 2 – 3 monthspapules which ulcerated later with raised borders usually at the site of the bite forming nodule.Regional lymphadenopathy, pain, pruritus and secondary infection.Immunity for both
No immunity
Heal with scar
No or minimal scars
Wet lesion
Dry lesion
Rapid necrosis
Slow evolution, less severe
Large 2 – 10 cm Small size
Usually single or few
Usually multiple
L. major
L. Tropica
CL
MUCOSAL LEISHMANIASIS:
It is caused by L. brasiliensis complex, cutaneous lesion may be fallowed by mucosal spread, metastatic lesions in the mucosa of the nose or mouth
MUCOSAL LEISHMANIASIS:
it characterized by thickening and erythema of the nasal mucosa at the junction of the nose and the upper lip, later ulceration will developed.ML.
No spontaneous healing and death may result from severe respiratory tract infection due to massive destruction of the pharynx
INVESTIGATIONS For cutaneous and mucosal leishmaniasis:
usually the diagnosis made on clinical characteristic of the lesionINVESTIGATIONS
Amastigotes can be demonstrated by slit skin smear stained by Giemsa stain. Leishmanin skin test is +ve except in those with diffuse CL. PCR is useful in both CL & ML.
TREATMENT of CL & ML
Small cutaneous lesion may heal spontaneously (( self – heal )) or byFreezing with liquid nitrogen.TREATMENT of CL & ML
Topical paromomycin and methyl benzathonium chloride is beneficial in CL. When the lesions are multiple or at disfiguring site, treatment with Sb 20mg/kg/day for 20 days.TREATMENT of CL & ML
Interalesional antimony 0.5 ml is rapidly effective, well tolerated and save. Fluconazole 200mg/day for 6 weeks reduce the healing time and cure 80% of CL caused by L. major.
TREATMENT of CL & ML
ML are treated with 28 days systemic Sb or 8 injections of pentamidine on alternated days regiem. Refractory CL or ML should be treated with amphotercin B .PREVENTION:
Personal protection against sandfly bites Use of insecticides No vaccine yet available.TOXOPLASMOSIS
Causative organism:Toxoplasma Gondii Congenital Tox. From infected mother during pregnancy to her fetus.Acquired Tox.
PATHOLOGY:
In congenital formthe parasite widely spread in the CNS, eyes, heart, lung and adrenals. If the infant survive, the parasite disappear from most organs except the brain (( CNS )) and retina.
In acquired form:
the organism invade the LN, spleen and less commonly; liver and myocardium.CLINICAL FEATURES:
Congenital Toxoplasmosis:
The main features are cerebral with hydrocephalus, microcephaly, convulsion, tremor or paralysis. Microphthalmos, nystagmus and choroidoretinitis are common.
Congenital Toxoplasmosis:
Hepatomegaly, thrombocytopenia and purpura may occurs. Severe forms are usually fatal and if the child survive, he will be disabled and blind. Mild cases presented with only choroidoretinitis.Acquired Toxoplasmosis:
Many of them are asymptomatic. In the acute form: Fever, cough, myalgia, malaise, maculopapular rash and rarely jaundice & myocarditis.In the chronic form:
Generalized lymphadenopathy, particularly cervical lymph nodes,may be spleenomegaly. Some pf them may developed encephalitis, myocarditis, pneumonia, hepatitis and even choroidoretenitis.