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Opportunistic infections in AIDS

Retno Wahyuningsih
Department of Parasitology Indonesia Christian University Faculty of Medicine

Opportunistic infection: def
infection caused by organism that in normal immuno-competent host does not caused disease, but in immuno - compromised host causes severe infection

HIV infection

Damage of immune system (AIDS phase) fails to overcome infections: immunocompromised. In AIDS the deficit of immune system is complex but in some extents presented by the decrease of CD4 count in the circulation

Repentigny et al. CMR 2004; 17: 729-59

Immuno-compromised host

Characterized by opportunistic infections Opportunistic infections:
 


parasites Virus bacteria fungus

Parasitic infections in immunocompromised host

Reactivation of old/dormant lesion
e.g. toxoplasmosis

Non pathogen parasites becomes pathogen
e.g. isosporiasis

Isospora sp. Blastocystis hominis Cyclospora cayetanensis Microsporidia . stercoralis Toxoplasma gondii Cryptosporidium sp.Parasites that cause OI Helminth Protozoa S.

 ingestion of oocyst. a serious often fatal infection in immunodeficient patients Mode of infection:  ingestion of raw or undercooked meat  contaminated water/ contaminated food. Occur in immunosuppresed invidual.  Organ transplantation  laboratory accident. AIDS.g.  trans-placental.Toxoplasma gondii  Toxoplamosis. e.   .

Toxoplasma gondii Definitive host is cat  asymptomatic in immunocompetent host  reactivate in immunocompromised host  Antibody against toxoplasma is prevalent world wide but clinical toxoplasmosis is less common until the pandemic of AIDS  One of the commonest opportunistic infections in AIDS.  .

Tachyzoit Rapidly dividing/transmitted form http://scienceblogs.com/afarensis/upload/2006/08/ToxoplasmaSB-a.jpg Bradizoit/cyst in muscle Slowly dividing/persist in tissue  reactivated .

95% is reactivation of latent infections as the result of progressive loss of cellular immune cells  CD4<0. (brain tumor) Jakarta: commonest cerebral disorder in AIDS .Signs and symptoms      pregnant woman: parasites may disseminate to the offspring AIDS: commonest clinical presentation is cerebral infection. seizures etc.1x109/L sub acute  acute confusional state with or without neurological defect Clinical manifestations: cranial nerve disturbances.

IgG & IgM  PCR: LCS.diagnosis  Laboratory test:  Clinical symptoms esp. blood . cerebral involvement (not specific)  Imaging: tumors with enhancing lesion (with contrast)  exjuvantibus  demonstration of the parasite in clinical materials (LCS-rare)  Serology to detect antibody.

Treatment      1st line therapy: combination of Pyrimethamine (50-75mg/day) and sulphadiazine 4-6g/day sulphadiazine induced rashes and fever are often happen in AIDS. . spiramycin. clarithromycin. roxithromycin and azythromycin (active against both form). Folic acid to counteract pyrimethamine on the marrow suppression Antibiotics: clyndamycin. Lifelong maintenance therapy to prevent relapse since the drugs unable to destroy cyst.

Prevention  Proper attention to hygiene  Avoid eat raw meat  cook meat (heating to 65°C kills the organisms)  Avoid cat feces. use gloves when cleaning cat litters and use disinfectants .

for the students only nice to know .Strongyloides stercoralis   strongyloidiasis tropical & subtropical regions  Man to man transmission  female parasitic. rhabditiform & filariform larvae in the intestine  filariform larvae: creeping eruption Rarely found in AIDS.

rhabditiform becomes filariform larvae in the intestine/perianal skin .filariform larvae penetrates the intestinal mucosa or perianal skin and continue its life cycle as the adult worm and cause chronic strongyloidiasis .Strongyloides stercoralis Autoinfection : .in immunocompromised host Hyperinfection: large amount of rh  filari .

transplantation. hematology malignancy  additional risk factors: DM. CRF. chronic alcohol consumption  AIDS is rare risk factor  . malnutrition.Strongyloides stercoralis Major risk factors: steroid therapy. HTLV-1 infection.

culture of specimen filariform larvae and and free living adults in culture Closed mouth part and end of tail .duodenal aspiration . stercoralis • Diagnosis rhabditiform larvae .S.fresh stool .

SS: Treatment & prevention  Albendazole 400 mg bid – 7 days or DOC: Ivermectine 200µg/kg daily 1-2 days for immunocompetent host (not available) Take care of risk factors.   .

Intestinal protozoa .

Similarities among Intestinal Spore-Forming Protozoa PATHOGENESIS OF DIARRHEA 1. secretion and motility Non ulcerative and non invasive ( except Microsporidia and Cryptosporidia) Pathology relates to the number of organisms 2. 3. . Infection inflammatory infiltrate  crypt hyperplasia and blunt of the villi  abnormalities in absorption.

modified of acid fast staining: Cryptosporidium. Light Microscopic stool examination 2. Fluorescent microscope : Cyclospora. Use of proper stains : .Similarities among Intestinal Spore-Forming Protozoa DIAGNOSIS 1.chromotrope : Microsporidia 3. Isospora . Cyclospora. Isospora .

jejunum and also in pancreas the surface of epithelial cells is its habitat and it able’ producing toxins .Cryptosporidium parvum     Host : man. animal MOI: ingestion of mature oocyst Pathology: living in alimentary tract system esp.

human:  immuno-competent: asymptomatic and self limiting  immunocompromized: . parvum: clinical symptoms   animal: cause diarrhea. self limiting but sometimes fatal. acuteprofuse diarrhea (12-17x/day fatal) .malnutrition .fatal in untreated case. .C.chronic diarrhea.

antibody detection (ELISA. parvum: diagnosis . Ziehl Nielsen staining . IFA) Direct stool exam.C.Demonstration of oocyst in stool (Ziehl Nielsen staining .

for one month Nitaxozamide water borne disease animal and man as reservoir host travelers diarrhea   .treatment  epidemiology    Strengthening the immune system by giving HAART Antibiotics: paromomycin 2535mg/kgbw.

symptoms  Could be asymptomatic  diarrhea and other gastrointestinal disturbances  fever  malaise .Cyclospora cayetanensis Host: man  MOI infection is ingestion of mature oocyst.  Pathology: living intracellular in jejunum enterocyte.

cayetanensis Diagnosis  oocyst in stool (ZN stain).C. seen as partially acid fast structure  easily infected by mature oocyst:   Treatment  trimethoprim 160 mg + sulfamethoxasole twice daily for 7 days Epidemiology: travelers diarrhea laboratory personnel people who take care patients .

C. cayetanensis .

nausea .    asymptomatic GIT: . .constipation etc. infection associated with: .enteritis.terminal ileitis. . immunocompromized host and animals.dysentry .Blastocystis hominis symptoms Host: man esp.diarrhea . .ulcerous colitis. MOI: ingestion of cyst in contaminated drinking water/food.

B. hominis: diagnosis  finding vacuolar forms in stool Treatment  metronidazole 3 x 750mg/dayfor 10 days Epidemiology  Travelers diarrhea .

: B. hominis .Stool prep.

belli & I.Coccidia : Isospora I. hominis  Size: 20-30 um Mature oocyst with 4 sporozoites in 2 sporocysts  MOI : ingestion of oocyst or sporocyst Clinical symptom: asymptomatic/ GIT complaints and self limiting in immunocompetent host   .

Hard to differentiate from bacteria & debris .MORPHOLOGY Isospora .Size : 20-30 um .Size : 1-2 um .Mature oocyst with 4 sporozoites in 2 sporocysts Microsporidia .

in AIDS patients:    fever malaise persistent diarrhea  death  Diagnosis: finding oocyst in stool .Isospora belli  Can cause severe disease esp.

2 weeks  Followed by maintenance 1X2 tab Check stool post treatment  .management  Cotrimoxazole 2X2 tab.

Prevention for intestinal protozoa Wash hand properly  Food handler  hygiene  Properly cooked dishes  Water treatment  resistant against chlorine filtration is suggested  .

Opportunistic infection caused by fungus/ Mycotic infection .

neoformans the most frequent cause of meningitis  cryptococcosis  H. capsulatum.Mycoses in AIDS major fungal infection are:  C. jiroveci cause infection in the lung & other organ  PCP  Cr. is dimorphic fungus that cause infection in untreated HIV infected patients who lives in endemic area  histoplasmosis . albicans (mostly) responsible for mucosal infections  candidosis  P.

pseudomembranous . remain problem in poor resources country  Repentigny et al.angular cheilitis. CMR 2004.erythematous . 200-400 cells/µL  clinical classifications: .Candidosis Oropharygeal candidosis (OPC)  most common fungal infection in AIDS  occurs when CD4 count ca. predictive for progression & onset of AIDS  decreased with the introduction of HAART. 17: 729-59 .

 limited food consumption which threaten the general health.OPC complicated by esophageal candidosis (EC)  CD4 count <200 cells/µL. CMR 2004.  Repentigny et al.  EC could be independent. 17: 729-59 .

Management: diagnosis OPC DD/ hairy leucoplakia  Laboratory test (oral swab): fungal element  EC  clinical. radiology and laboratory.. Bull WHO 2005. 83: 700-6 . but laboratory sample must be taken by endoscope Coogan et al.

Management: therapy  Good oral hygiene is important  Topical   antifungal for 2 weeks nystatin Amphoterin B lozenges fluconazole (DOI)  Oral: .

33%  Prevalence: Casadeval 2003.yptococcus  AIDS:  Risk : inhalation of spore the most common clinical manifestations is meningitis factors: CD4 < 50-100 cells/µL in Jakarta ca. data Lab Parasitology FKUI .Cryptococcosis  Cr. Dupont et al 2003.

seldom acute with fever and head ache as the most common symptoms More symptoms will manifest with time Altered mental status and fever is suggestive for meningoencephalitis Dissemination to other organ is possible including skin Casadeval 2003. Dupont et al 2003. Wahyuningsih et al .Cryptococcosis     Meningitis: subacute.

Wahyuningsih.diagnosis Culture on SDA Direct examination india ink: CSF from AIDS patient with meningitis  encapsulated yeast Serology: detect GXM antigen Picture: R. Dept. Parasitol FKUI .

the aim is to prevent CNS cryptococcosis by giving antifungal tretament Saag et al CID 30:710-8 .Therapy:      Amphotericin B + 5FC first line of therapy for cryptococcal meningitis Continued by the application of fluconazole In the management of cryptococcosis the CSF investigation is mandatory LP is mandatory in meningitis In cryptococcosis outside CNS.

endemic mycosis. true pathogenic In nature: saprophytic mould.    Environment: avian dropping and bat guano Infection: inhalation of microconidia & causes primary histoplasmosis in the lung which in immunocompetent host is self limiting with calcification. a thermally dimorphic fungi. capsulatum. produces microconidia. .histoplasmosis  Caused by H.

Clin Mycol 2003 . skin lesion Cited from Kauffman. weight loss. pneumonia. sweats.Histoplasmosis in AIDS: pathogenesis From lung disseminates throughout the body via RES mostly reactivation of old lesion  fever. fatigue.

grow slowly.Diagnosis • Biopsy: direct exams – giemsa stain • Intracellular yeast (arrow) Culture on SDA: Whitish filamentous colony at room temperature. 3-4 weeks .

classic coca cola or pepsi cola   Cited from: Como & Dismukes Clin Mycol 2003 . with anti TB. To increase the bioavailability of itraconazole it must be taken with high fat meal or acidic beverage e.g.Therapy:  1st line therapy is amphotericin B then continued by itraconazole Critical point in therapy is low absorption of itraconazole and its interaction with many agents esp.

Pneumocystis Pneumonia (PCP)      P. CD4 ≥ 200 cells/µL MOI: inhalation? Symptoms: fever. substernal chest tightness and shortness of breath Cited from Decker & Masur Clin Mycol 2003 . non productive cough. dyspnea. jiroveci : no ergosterol as wall component Not cultivated in vitro  life cycle has not been fully elucidated.

immunofluoresence  .Diagnosis & its constrain Not cultivable  no media available  Found organism in clinical materials Gold standard is GMS  the most relevance clinical materials is BAL which needs bronchoscopy  induced sputum is simple. sensitive and noninvasive  Monoclonal AB .

symetrical insterstitial markings.PCP: diagnosis  Based on clinical symptoms (non specific) Chest radiograph: diffuse. CT scan ground glass appearance Laboratory: demonstration of the organism in clinical materials   .

PCP dengan pewarnaan Giemsa .

(p.v.o line Dapsone 100 mg/day (p.PCP: treatment  1st line: TMP-SMX     2nd    TMP: 15-20 mg/kg/day SMX 75-100 mg/kg/day i.v/p. max 300 mg/day .TMP 15-20 mg/kg/day.).) tid Pentamidine isethionate (i.o/i.o.o.) 4 mg/kg/day.v) Atovaquone 750 mg (p.