Parasitic infections of CNS microbiology.pptx

Parasitic infections of cns is very important and very useful topic of microbiology.

1. Many parasitic infections can affect the human CNS(Brain , Spinal Cord and eye). Some affect the CNS as their primary Infection site and few as ectopic site of infections Parasitic Pathogenic agents which mainly infect CNS are : 1. Protozoans : (a) Free – Living Amoeba infections of CNS ( Naegleria Fowleri , Acanthamoeba Sp. And Balmuthia and Sappinia ) (b)Toxoplasma encephalitis ( Toxoplasma gondii ) (c)Cerebral Malaria ( Plasmodium Falciparum ) 2. Cestode : (a) Neurocycticercosis ( Taenia solium ) 3. Trematode :™ (a) Schistosoma mansoni and S. japonicum infections (b)Cerebral paragonimiasis 4. Nematode : (a) Hyperstrongyloidiasis syndrome ( Strongyloides ) (b)Eosinophilic meningitis ( Angiostrongylus cantonensis ) Parasitic Infections Of CNS INTRODUCTION :

2. Free-living amoeba Typically found in warm fresh water, such as ponds, lakes, rivers and swimming pools. It exists in nature as cyst and trophozoite forms. Trophozoite stage: The trophozoites occur in two forms : Amoeboid (20 μm )and Flagellated form (10-18 μm ) Cyst stage: Cysts measure 7–15 µm in size and is surrounded by a thick, smooth double wall. It is found in the environment Till now more than 300 cases of PAM have been reported; mainly from USA (>100 cases) and also from other parts of the world. In India, it is reported from Mangalore, Kolkata and Rajasthan (>20 cases reported so far). Free Living Amoeba Infections Of CNS Naegleria fowleri INTRODUCTION : MORPHOLOGY : EPIDEMIOLOGY:

3. Infective form: Amoeboid form is the invasive and infective form of the parasite Mode of transmission: Man acquires infection by nasal contamination during swimming CNS invasion: The amoeboid form invades the nasal mucosa, cribriform plate and travels along the olfactory nerve to reach brain. The penetration initially results in significant necrosis of the nasal mucosa and olfactory bulbs. Tissue destruction is mainly mediated by two mechanisms: 1. Direct ingestion of the brain tissue. 2. Contact dependent cytolysis mediated by hemolytic proteins, cytolysins and phospholipase. PATHOGENESIS / LIFE CYCLE :

4. Primary amoebic encephalitis (PAM) is caused by N. fowleri . The incubation period ranges from 1 to 14 days . It is rapidly progressive and results in fatal destruction of brain tissue. Initial Symptoms : Headache , fever , lethargy , nausea , vomiting , rhinitis and disorientation are present. Later Symptoms : Patient declines rapidly , becomes comatose and dies within 7 -10 days CLINICAL MANIFESTATION :

5. CSF is the specimen of choice. CSF analysis : CSF is thick purulent, with pus cells >20,000/µL, elevated protein and reduced sugar level . CSF microscopy: Detection of characteristic trophozoites in CSF confirms the diagnosis. Histopathology: Brain biopsied tissue may be stained with hematoxylin and eosin and Giemsa stain to demonstrate trophozoites having sky blue cytoplasm with a pink nucleus Culture: CSF sample can be cultivated on non-nutrient agar (Page’s saline and 1.5% agar), lawn cultured with bacterial supplement like E. coli. Naegleria feeds on bacteria and crawls over the lawn culture of E. coli to produce trails (Trail sign) Molecular methods: Multiplex real-time PCR is available targeting three regions of 18S rRNA of Acanthamoeba species, Balamuthia, and N. fowleri in CSF Imaging methods: CT scan and MRI show obliteration of cisterns, and diffuse enhancement around midbrain, subarachnoid space and over cerebrum LABORATORY DIAGNOSIS :

6. No effective treatment is available for PAM. Amphotericin B has considerable anti-Naegleria effect. The Prognosis is very poor. TREATMENT AND CONTROL:

7. Acanthamoeba species are free-living amoebae that infect CNS, skin and eye. They are ubiquitous and present worldwide. It is so named because of the spine like pseudopodia present in trophozoite (called as acanthopodia) Reservoir for bacteria: Acanthamoeba may harbor bacterial pathogens such as Legionella and may serve as a potential reservoir and act as Trojan horse of the microbial world. Acanthamoeba species exist in nature as cyst and trophozoite forms. There is no flagellated form. Acanthamoeba Infections INRODUCTION : MORPHOLOGY :

8. Man acquires infection by inhalation of aerosol contaminated with cyst or trophozoite. Primary sites of infection are sinuses and lungs. From lungs, trophozoites reach CNS by hematogenous route It causes two important clinical syndromes 1.GAE (granulomatous amoebic encephalitis) in immunocompromised patients like HIV positive patients, and 2. Keratitis among contact lens users LIFE CYCLE :

9. (1) GRANULOMATOUS AMOEBIC ENCEPHALITIS (GAE) : Incubation period varies from several weeks to months. Subacute to chronic course Pathology: It produces focal granulomatous lesions in brain and Lymphocytosis of CSF can be seen. Epidemiology: More than 400 cases of GAE due to Acanthamoeba have been reported so far In addition to GAE, Acanthamoeba produces nasal ulcers, cutaneous ulcers and musculoskeletal abscesses. (2) AMOEBIC KERATITIS : Acanthamoeba enters the cornea through minor abrasions present on the cornea . The resultant infection is known as Amoebic keratitis . It is painful Condition produces corneal ulcerations , iritis , scleritis , hypopyon and can lead to loss of vision . (3) SKIN LESIONS : Cutaneous ulcers, musculoskeletal abscesses , sinusitis and nasal ulcers are seen in HIV patient . CLINICAL MANIFESTATIONS:

10. CSF microscopy: CSF is the specimen of choice for GAE. It should be examined immediately. Presence of characteristic trophozoites (or occasionally cyst) confirms the diagnosis. Wet mount examination and phase contrast microscopy are performed Culture: Clinical specimens are inoculated onto nonnutrient agar with bacterial supplement, and incubated at 30°C. However, unlike Naegleria, Acanthamoeba is not readily isolated from culture Molecular methods: Multiplex real-time PCR is available targeting three regions of 18S rRNA of Acanthamoeba species, Balamuthia, and N. fowleri in CSF Imaging method: CT scan or MRI reveals spaceoccupying or ring enhancing lesions LAB DIAGNOSIS :

11. Unfortunately, there are no therapies with proven efficacy against this disease. Only three cases have survived so far The combination therapy recommended include pentamidine , an azole, sulfonamide (e.g. cotrimoxazole) and possibly flucytosine. TREATMENT :

12. Toxoplasma Encephalitis INTRODUCTION : Toxoplasma gondii is an obligate intracellular parasite Human infection is quite common But disease progresses to only immunocompromised individual MORPHOLOGY :

13. Toxoplasma gondii exists in three morphological forms : (1) TACHYZOITE: Actively multiplying form Crescent shaped Seen in acute infection (2) TISSUE CYST   Resting stage of the parasite Seen in chronic infections most common site is muscles and brain Inside the cyst slowly multiplying trophozoites are called as bradyzoites BRADYZOITE: Resistant to gastric juice ; Multiplies slowly ; Contains PAS positive amylopectin granules (3) Oocyst : Sexual form of the parasite found only in cats and felines

14. LIFE CYCLE :

15. CLINICAL MANIFESTATIONS :

16. LAB DIAGNOSIS :

17. Congenital toxoplasmosis: oral pyrimethamine (1mg/kg) and sulfadiazine ( 100mg/kg) with folinic acid daily for one year.  Toxoplasmosis in AIDS : Cotrimoxazole Dapsone – Pyrimethamine Atovaquone with pyrimethamine TREATMENT :

18. Taenia solium , the pork tapeworm, belongs to the cestode family Taeniidae. Neurocysticercosis (NCC) is a neurologic infection caused by the larval stage of the tapeworm. Humans get infected with T.solium when they consume green and leafy vegetables contaminated with the eggs of the tapeworm. They may also acquire the infection through autoinfection , wherein the eggs are ingested either from the contaminated hands of the infected human or by reverse peristalsis. . Neurocysticercosis INTRODUCTION:

19. India : Cysticercosis is highly prevalent in the northern states such as Bihar, Odisha, Uttar Pradesh and Punjab. It is believed that NCC is largely underreported in India, accounting for 2–3% of epileptic cases . The underreporting is because of lack of systematic population-based studies and unavailability of imaging techniques in rural areas. EPIDEMIOLOGY :

20. Life cycle of T. solium causing cysticercosis is different than its life cycle when it causes intestinal taeniasis . Host: Man acts as both definitive and intermediate host Infective stage: Eggs of T. solium Mode of transmission: Firstly man acquires the infection by—(1) ingestion of contaminated food or water containing eggs of T. solium , and (2) autoinfection Human cycle: The embryo or oncosphere is released from the eggs, penetrates the intestine and enters into the portal circulation or mesenteric lymphatics and reaches to various organs like subcutaneous tissue, muscle, eye and brain where it is transformed to the larval stage i.e., cysticercus cellulosae in 7–9 weeks and deposited as cyst. Full development to mature cysts takes 2–3 months of time. LIFE CYCLE :

21. Clinical spectra of the disease depend upon the localization of the cyst. Though it is discovered from any site of the body, but the common sites are CNS , subcutaneous tissue , skeletal muscle and eyes . NCC is considered as the most common parasitic CNS infection of man and the most common cause of adult onset epilepsy throughout the world. Other clinical features include: 1. Increased intracranial pressure and hypertension . 2.Chronic meningitis 3.Focal neurological deficits 4.Psychological disorders and dementia 5. Cerebral arteritis (associated with subarachnoid cysticercosis) 6.Basal and ventricular involvement: Carries poor prognosis Clinical Manifestation:

22. Radiodiagnosis —CT scan and MRI (useful for detecting number, location, size of the cysticerci and the stage of the disease) Antibody detection in serum or CSF— 1. ELISA (using crude extract of cysticerci ) 2. Western blot (using 13 kDa LLGP Ag) Antigen detection in serum or CSF—ELISA Lymphocyte transformation test Histopathology of muscles, eyes, subcutaneous tissues or brain biopsies—can detect cysticerci Fundoscopy of eye —detects larvae Modified Del Brutto diagnostic criteria : It is based on clinical, imaging, immunological and epidemiological data LAB DIAGNOSIS :

23. Antiparasitic agents: Albendazole or praziquantel are theDrug of Choice Symptomatic treatment : 1.Seizures by antiepileptic drugs 2.Hydrocephalus: Attempts should be made to reduce intracranial pressure. Surgery: 1.Open craniotomy to remove cysticerci is rarely required nowadays 2.Surgery is indicated for ocular, spinal and ventricular lesions because antiparasitic drugs can provoke irreversible inflammatory damage TREATMENT :

24. Cerebral malaria (Plasmodium falciparum) African sleeping sickness (Trypanosoma brucei) Chagas’ disease (Trypanosoma cruzi ) Cerebral amoebiasis (E. histolytica) Rare Diseases

25. Fungal infections are rarely seen in healthy individual as they rarely gain entry . Seen in immunocompromised individual. Route of Entry (Hematogenous route from a primary site ) : 1.Lungs 2.sinus and 3 .mastoid or internal auditory meatus . Fungal Infections of CNS

26. CNS infections by candida are invariably due to the hematogenous spread of the organism . Such infections are commonly caused by Candida albicans which can produce acute or chronic meningitis or meningocephalitis . Fever , meningism and localized neurological signs Microscopic examination of CSF shows pleocytosis . Gram stain may show budding yeast cells 3. Culture on blood agar or SDA and Speciation confirms the diagnosis . Amphotericin B with Flucytosine Candida CLINICAL FEATURE LAB DIAGNOSIS : TREATMENT : INTRODUCTION :

27. Most common fungal agent causing meningoencephalitis , space – occupying lesions and chronic meningitis in immunocompromised individual . The two most common Sp. are : Cryptococcus neoformans var neoformans and Cryptococcus neoformans var gatti . Fever , chronic headache , malaise , lethargy , nausea and vomiting . Microscopy : Stained with INDIA INK to visualise capsulated yeast cells. 2. Culture : Specimens are inoculated on SDA for growth and speciation . Serology : The Capsular polysaccharide antigen of Cryptococcus is detected by latex agglutination or enzyme immunoassays from CSF , serum or Urine . Fluconazole , amphotericin B with Flucytosine . Cryptococcus CLINICAL FEATURE LAB DIAGNOSIS : TREATMENT : INTRODUCTION :

28. Causes Histoplasmosis in immunocompromised patient . Can also cause acute to chronic meningitis or may manifest as cerebrovascular accident due to infective emboli . Fever , headache , confusion and lethargy . Meningeal irritation and cranial nerve palsy may also be seen Diagnosis is based on CSF analysis for increased protein and culture , which often yields Histoplasma capsulatum . MRI and other imaging technique may also be helpful . Amphotericin B , itraconazole or Fluconazole . Histoplasma CLINICAL FEATURE LAB DIAGNOSIS : TREATMENT : INTRODUCTION :

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