Pastest: Infectious disease Flashcards

Question

Jaundice \>\>\> Dx

Answer 1

* Hepatosplenomegaly + _mild high AST/ALT, **very high bilirubin,** very high creatinin_e \>\>\> Dx: Leptospirosis (Weil's disease) \> TOC: IV Penicillin * **_Sewage worker_** \>\>\> Dx: Leptospirosis * **_Fishing trip_**, arthralgia, myalgia, **_dry cough,_** jaundiced sclera \>\>\> Dx: Leptospirosis * Travel by river side, **_Very high bilirubin_**, mild high creatinine, very high ALT, very high ALP \>\>\> Dx: Leptospirosis * may also have purpuric rash, scattered coarse crackles on auscultation, RUQ pain * Possibility of exposure to 'rat urine' near the river bank * **Course of leptospisosis:** After 2 to 30days of incubation period \>\>\> abrupt onset of 'flu-like symptoms' \>\>\> After 5-days of that illness \>\>\> jaundice, coagulopathy * Tx: Doxycycline, Penicillin, Cephalosporin & measures to reduce the rodent population * Incubation 2-6 weeks \>\>\> Flu-like illness (fever, malaise, anorexia, nausea. myalgia) \> then, more prominent rise of AST/ALT, high bilirubin, **_normal creatinine_** \>\>\> Dx: HAV * **Africa, South america emdemic region** * high AST/ALT, high bilirubin, fever, pharyngitis, lymphocytosis, anaemia +/- hepatosplenomegaly + **_immunocompromised/HIV/renal transplant_** \>\>\> Dx: CMV * high AST/ALT, high bilirubin, fever, pharyngitis, _LNpathy_, lymphocytosis, +/- hepatosplenomegaly \>\>\> Dx: EBV * Hepatomegaly + Ascites + Abdominal pain + NO fever \>\>\> Dx: Budd-Chiari syndrome (occlusion of draining hepatic veins) * Bloody diarrhoea + anaemia + Low platelets + deranged LFTs (= hepatic injury) \>\>\> Enterotoxigenic E. coli O157 (= Haemolytic uraemic syndrome = HUS) * Microangiopathic intravascular haemolytic anaemia

Answer 2

Interferon-alpha (IFN-alpha) [S/C] \>\>\> * Flu * Depression, emotional lability, mood changes * Fatigue * Thyroiditis * Low WBC (Leukopaenia) * Low platelet (Thrombocytopaenia) Ribavirin PO \>\>\> * Haemolytic anaemia (most common S/E), cough * reduces Hb up to 20g/L \> so, it is avoided in \> * Previous h/o blood disorder * Elderly * Heart disease * Teratogenic (prevent pg during & up to 1 year from Tx; some say 6months, whatever sex is being treated) \* Viral genotype 2, 3, 3a (chronic infection) are more likely to respond to Rx \* genotype 4 has less responsiveness \* Telepravir for HCV can cause hypocalcaemia \* Rx response is checked by ALT level and viral load \* HCV can raise AST/ALT transaminases & creatinine (by GN); these are not by drugs

Answer 3

* Annual influenzae vaccine (yearly basis- against influenzae virus (not against haemophilus influenzae type B = Hib) * 5-yearly pneumococcal vaccine (Against streptococcus pneumoniae) \*\*\* influenzae vaccine needed in annually post-splenectomy patient is also against influenzae virus (not against Hib; Hib vaccine against type haemophilus influenzae B is given 14days after emergency splenectomy or 14days = 2weeks before elective splenectomy)

Answer 4

* Patients in chronic care facilities (e.g. especially the elderly) * Chronic cardiopulmonary, lung disease, renal disease, diabetes mellitus, haemoglobinopathies * the immunocompromised * post-splenectomy

Answer 5

* Incubation period = over 1 week; p. falciparum has shorter, others 1-2weeks; can occur over several weeks \> however, over several months (if partially treated) * Duffy antigen in RBC is protective against \>\>\> P. vivax * Vector: Anopheles mosquito * Liver hypnozoites is formed by \>\>\> P. vivax and P. ovale (not by falciparum) * Life cycle present in P. vivax, but not in falciparum ? \>\>\> Liver hypnozoites \*\*\* Aedes is the vector for \> dengue. yellow fever. Zika virus

Answer 6

* All forms of malaria create gametocytes \>\>\> taken up by the mosquito \>\>\> go onto develop oocytes and \>\>\> eventually, sporozoites \>\>\> injected in to human host * After initial invasion and development of schizonts in the liver \>\>\> rupture \>\>\> releases merozoites in blood stream \>\>\> go and infect erythrocytes \>\>\> replicate in RBC & rupture \>\>\> releases further merozoites * Before rupture and propagation of the erythrocytic stage \>\>\> the form within erythrocytes = trophozoites: immature are the risng-stage, then followed by mature erythrocytes * Liver hypnozoites are dormant stage in liver (for P. vivax & P. ovale = benign malaria) \>\>\> can reactivate after a signifcant time \>\>\> lead to relapse * Liver hypnozoites are not seen in falciparum * TOC to eradicate liver hypnozoites \>\>\> primaquine (given only in vivax and ovale) * If we give quinine therapy in falciparum (TOC: Artesunate) \>\>\> NO need to give primaquine \>\>\> give fansider (pyrimethamine + sulfadoxine) or tetracycline \>\>\> cover the possibility of low-grade quinine resistance *

Answer 7

Gram +ve cocci: * Chains/ Pairs * Streptococci * Clusters * Staphylococci * Enterococci * Catalae +ve \>\>\> Streptococci * No haemolysis \>\>\> Enterococcus * Partial haemolysis (green) \>\>\> alpha-haemolytic = S. pneumoniae, S. viridans * Complete haemolysis (clear) \>\>\> beta-haemolytic = S. pyogens (group A), S. agalactae (group B) * Catalase -ve \>\>\> Staphylococci * Coagulase +ve *(when added to diluted plasma \> coagulation of fibrinogen to fibrin clot) \>\>\> S. aureus* * *Coagulase -ve \>\>\> S. epidermidis, S. saprophyticus*

Answer 8

* Normal B lymphocyte count, but increased number of plasma cells = polyclonal B cell activation \> polyclonal hypergammaglobinaemia * Hypergammaglobinaemia (polyclonal) + increase across Ig classes * Depletion of CD4+ T cells (N: 300-1300 X10⁶/L) * Defecient T cell response to antigenic stimuli \> mainly to soluble antigen and mitogenic substances, such as phytohaemoagglutinin, concanavalin A * Defective natural killer cell function & decreased number * Delayed hypersensitivity reaction (e.g. type IV) * IBM-DELL * Increased B2-microglobulin * Decreased IL-2 production

Answer 9

* Sickle cell anaemia patient \>\>\> infected with parvovirus B19 \>\>\> aplastic crisis * Erythematous rash all over body * Painful swollen joints * Absent reticulocytes

Answer 10

Thrombocytopaenia in malaria: * Occurs in falciparum and vivax malaria * Associated with \> severity of disease & renal impairment * Treat only if - \> * Platelets \<30 + active bleeding OR * Platelets \<20 +/- bleeding (as a prophylactic therapy) * TOC: Platelet transfusion * If not such 2 criteria \> Do nothing in respect of platelet count \*\*\* Treatment of severe malaria or falciparum malaria \> Artemesinin (its not a tx in respect to thrombocytopaenia) \*\*\* Eltrombopag is Tx of thrombocytopaeia with refactory ITP \*\*\* FFP is NOT Tx of thrombocytopaenia

Answer 11

* Warfarin toxicity * Massive BT * AT-III deficiency * Immunodeficiencies * where we need to replace isolated clotting factors \* It is NOT a treatment of thrombocytopaenia

Answer 12

* Exotoxin production * It causes progressive descending weakness of botulism * Botulinum exotoxin is broken down in to 7 neurotoxins \>\>\> A, B, C (C1, C2), D, E, F, G = they have distinct antigenic & serological profiles, but structurally similar * Human botulism is caused by: A, B, E, rarely F * Extotoxin means it's secreted \*\*\* Nerve infiltration is caused by \> HSV, Shingles \*\*\* Stimulation of Ach release by \> Latrotoxins (from some black spiders) \> these stimulates Ach release from NMJ, until vesicles are depleted \>\> causing 'paralysis' \*\*\* Endotoxin is produced by \> Gram -ve bacteria (outer membrane of cell wall) [NO muscle weakness/paralysis]

Answer 13

* Features: palpable purpura, papule, urticaria, vesicle, tiny papules * Caused by: **_HCV, HIV, beta-haemolytic streptococcus_**

Answer 14

* Trip to Africa \> think \> African Tick bite fever: * Fever, myalgia, arthralgia, maculopapular rash, bite sign, blackened core, surrounded by erythema * + milder disease, normal WBC, normal platelet \>\>\> Dx: **Rickettsia Africae** * + more severe disease, low WBC, low platelets \>\>\> Dx: **Rickettsia conorii (Mediterranean spotted fever)** * TOC for both: Doxycycline for 2 weeks * Spread by mites of wild rodents and mites \> * Flu like illness + at bite site: black crusty scab \>\>\> Dx: **R. akari (Rickettsial pox)** * Exposure \> after 2 weeks \> flu-like illness + rash: spreading from trunk to arms + NOT involved palm, sole, face +/- meningoencephalitis \>\>\> Dx: **R. prowazekii (epidemic typhus)** * Travelling to USA \> animal/human host \> fever, rash, myalgia, _nausea. vomiting, confusion_ \>\>\> D/D: Ehrlichia chaffeensis * Exposure to _water_ \> anorexia, fever, _depression, diarrhoea,_ NO rash \>\>\> D/D: Neorickettsia sennetsu (= gm -ve bacteria, spread through trematodes) \> Potomac horse fever

Answer 15

* All hepatitis \>\>\> very high ALT, ALP, Biliturbin, * Travelling \>\>\> HAV, HEV * Pregnant woman have more risk * Previous vaccination rules out HAV (2 vaccinations give complete protection) * IV drug use \>\>\> HBV, HCV, HDV * Clean needle use \>\>\> rules out them * HBsAg -ve, HBV DNA -ve +/- HBeAg -ve \>\>\> rules out active acute hepatitis * Absence of HBV \>\>\> rules out HDV

Answer 16

* Albendazole 400mg BD for 3days, repeated after 3 weeks *OR* * Ivermectin * If itching \> Anti-histamine * Response: Tx usually clears the worm, but in endemic areas \> re-infection is common

Answer 17

* Nitazoxanide * Cryptosporidium causes self-limiting gastroenteritis

Answer 18

* Tinidazole * Flagellated protozoon \> faeco-oral spread \> infection of _duidenum and jejunum_ \> _explosive diarrhoea_, abdominal pain, _flatulence_ + malabsorption \> _weight loss_

Answer 19

* Sulfadiazine/Pyrimethamine + Folinic acid * Run for several weeks * Pyrimethamine is a folate antagonist \>\>\> So, add folinic acid supplementation + regular (weekly) blood counts * After initial Tx \> long term secondary prophylaxis is also important * If sulfadiazine is NOT tolerated \>\>\> Give pyramethamine + * Clindamycin OR Clarithromycin OR Azuthromycin * So, It is not the first line

Answer 20

In case of non-pregnant individuals: (C.I in pregnancy) * Neurosyphilis * Lyme disease * Rickettsial infection

Answer 21

* In immunocompromised individuals with \> * CMV * Mucocutaneous HSV

Answer 22

From tick bite \> * Before 6months \> Borrelia IgM * peaks after 6-8weeks \> disappears after 6months * After 6months \> Borrelia IgG * Less commonly \> PCR _(from skin samle, not in blood)_

Answer 23

* Anti-retroviral therapy \> immune-reconstitution syndrome \> improve reponse to HBV vaccination * HIV positivity \> Inadequate response to HBV response; Factors of oor response maybe - * Increasing age * Decreasing CD4 count * Increased HIV viral load \*\*\* HCV/HAV infection or vaccination has NO effect on HBV vaccination

Answer 24

* Specific (most suggestive): * elevated 1,3-beta-D glucan levels (BDG) * BDG is present in the walls of invasive fungii, also in PCJ cysts * It is currently underdevelopment as a screening option for PCJ pneumonia * Non-specific: (= present in many other conditions) * High LDH * CT thorax: ground glass infiltration * CXR: patchy consolidation Treatment of PCJ pneumonia: IV Co-trimoxazole Alternative: Pentamidine

Answer 25

* Transmitted by: * consumption of infected water (contaminated with cat faeces) * consumption of infected food \> undercooked meat of sheep and goat (contaminated with cat faeces) * Cats are commonly implicated in its epidemiology * Life cycle is completed in gut of cat * Immunocompetent individuals \>\>\> asymptomatic or very mild transient illness * Immunocompromised individuals (particularly HIV + low CD4 count) \>\>\> fulminant disease process * Human can pass one to another by \> vertical transmission * IOC: DAT (Direct agglutination test) to detect IgG antibodies of toxoplasma gondii *_(do NOT detect IgM here)_* * Eye manifestations are common * HIV doesn't cause primary infection of toxoplasma \> It causes secondary infection by 'reactivation'

Answer 26

* Normochromic normocytic anaemia (due to HIV) * Reactive plasmacytosis \> * Polyclonal hypergammaglobinemia * Thrombocytopenia (due to HIV) * Lymphopenia (due to HIV seroconversion) * Macrocytosis (Macrocytic anaemia)- due to Zidovudine * Pancytopenia (due to Zidovudine) * Hyperlactataemia (due to didanosine, stavudine) * Lactic acidosis (due to Tenofovir) * Hyperlipidaemia (due to protease inhibitors) * Hyperblirubinaemia (due to indinavir)

Answer 27

Factors which reduce vertical transmission (from 25-30% to 2%) * Maternal antiretroviral therapy (from 28weeks onwards) * Mode of delivery (caesarean section) * Neonatal antiretroviral therapy - Zidovudine - **the most effecttive measure** among all 4. * Start IV infusion at the onset of labour \>\>\> continue in the neonate up to 6 weeks of age * If it is not continued up to 6weeks in neonate, only IV infusion at labour has less evidence to support \> so must continue up to 6weeks of neonate * Infant feeding (bottle feeding) * Avoid breast feeding in all cases, even if mother is taking anti-retrovirals

Answer 28

* Painful: Herpes, Chanchroid * Both can be multiple * Shallow ulcer \> Herpes * Crops of vesicles (later goes erosion into ulcer) \> Herpes * Shooting pain, urethral discharge, flu \> Herpes * Gm stain: -ve (no growth/no organism) \> Herpes * Bilateral tender inguinal lymphadenopathy \> Herpes * Unilateral inguinal lymphadenopathy (often suppurate) \> Chancroid * Ragged edge ulcer, bleeds easily on touch \> Chancroid * Grey, yellow purulent exudates \> Chancroid * Erythematous papules, breaks into painful ulcer \> Chancroid * Giant serpiginous ulcer \> Chancroid * Prepuce, frenulum of male \> Chancroid * Vaginal entrance \> Herpes/Chancroid * Perineum in female \> Chancroid * Gm stain: Gm -ve rods \> Chancroid * Africa \> Chancroid (but rely mainly on features) * Herpes is caused by HSV-2 \> HSV-1 now * Chancroid is caused by haemophilus ducreyi \> IOC: take swab from the lesion \> culture on chocolate based media \> TOC: single dose Azithromycin, IM ceftriaxone, or 7-days of Erythromycin * Painless: Syphilis, Lymphogranuloma venereum, Granuloma inguinale * Painless solitary lesion +/- Painless inguinal lymphadenopathy \> Primary Syphilis * Painless papule/ulcer + later, painful inguinal lymphadenopathies (buboes) \> Lymphogranuloma venereum * Africa, travel to African countries, Papua New Guinea \> Granuloma inguinale (but rely mainly on features) * Indurated nodules \> Granuloma inguinale * Spreading/large ulcer, friable edge \> Granuloma inguinale * Getting progressively large \> Granuloma inguinale * Primary chancre of syphilis heals gradually, where klebsiella granulomatis is gradually enlarging * Syphilis is caused by treponema pallidum, Lymphogranuloma venereum is caused by chlamydia trachomitis, Granuloma inguinale is caused by - Klebsiella granulomatis * Chlamydia trachomatis has different serovars: D to K is extremely available in the UK \> urethritis, urethral discharge; L1-3 is an increasing problem \> LGV (mainly in male homosexuals); LGV Lnpathy can ulcerate & be locally destructive

Answer 29

* The most common: Cryptosporidium *(not cryptococcus neoformans- that most commonly affect respiratory & CNS, less commonly skin, prostate, medullary cavities of bone, never GIT) \>\> remember, both 2 most common organism has **_spore_** in them* * Second common: Microsporidium * CD4 50 to 300 \>\>\> Cryptosporidium * Profuse watery (non-bloody diarrhoea) + microscopy of stool sample: oocysts on (ZN staining) \>\>\> Cryptosporidium \>\>\> **_TOC: Anti-retroviral therapy (ART)_** * **TB \> having various presentation \> can also have diarrhoea \> BUT, ZN stain shows AFB** (NOT oocytes) * Very advanced HIV (CD4 \<100) + bloody diarrhoea \>\>\> CMV \>\>\> TOC: IV Ganiciclovir * CD4 \<50 \>\>\> Microsporidium * Bloody diarrhoea + gm stain: gm-ve rod \>\>\> Dx: Salmonella * Large volume watery diarrhoea (= small bowel diarrhoea) \>\>\> Microsporidium, Salmonella * Microsporidum \>\>\> more common than Salmonella * Salmonella needs h/o eating/travelling, fever; can be watery/bloody \*\*\* HIV patient + very recent history (days) of anal inter-course \>\> bloody diarrhoea with mucous \>\>\> Dx: Shigella * Cryptosporidium has profuse watery diarrhoea * Microsporidum has large volume watery diarrhoea * CMV has bloody diarrhoea but + need more long time to develop + CD4 \<100 \*\*\* In patients with HIV + diarrhoea + CD4 \<100 \>\>\> IOC: Colonoscopy with ileal intubation

Answer 30

Causes of lipoatrophy/lipodystrophy in HIV: * Stavudine (most common) * Mx: Switch Stavudine to another agent Causes of dyslipidaemia/hyperlipidaemia/isolated hypertriglyceridaemia: * Protease inhibitors * Mx: Start pravastatine (As it is NOT metabolised by Cytochrome p450, not affected by protease inhibitors or Nevirapine) \> Protease inhibitor is an inhibitor and Nevirapine is an inducer If both Lipoatrophy + dyslipidaemia: * Mx: Switch stavudin into another agent + start pravastatin

Answer 31

Cause of rash while on anti-retrovirals and Anti-TB drugs: 1. Nevirapine (NNRTI) \> widespread, maculopapular rash, itchy 2. IRIS (Immune Reconstitution Inflammatory syndrome) \> paradoxical worsening of other infections (including TB) : *It is a Dx of exclusion; So first exclude drug reactions \> then consider* 3. Kaposi sarcoma \> Flat, purple skin lesions -\> progress to plaques/nodules (NOT widespread, NOT itchy), most common in: skin of face, mucosa of GI and respiratory 4. Rifampicin, Zidovudine (Less common)

Answer 32

*(From the table list of Hamad, same)*

Answer 33

* Dx: Candidiasis (mainly occurs in advanced HIV, with very low CD4 count) * **Tx: First best step: Oral Fluconazole for 14days** * If symptoms do NOT improve after this \>\> _only then_ Endoscopy (Oesophagogastroduodenoscopy) * Do NOT start anti-retroviral therapy before treating candidiasis, although it is newly diagnosed (can be started after that). First consideration is to treat the opportunistic infection * In this advanced HIV \> D/D or alternative of candidiasis are: CMV, HSV

Answer 34

* **_Repeat blood glucose testing_** * Quinine \>\>\> (+) insulin release \>\>\> due to extreme ctabolism a/w malaria infection \>\>\> glycogen stores rapidly deplete \>\>\> severe hypoglycaemia * So, **_first step is to repeat blood glucose leve & every 2-hourly_** \>\>\> once confirmed hypoglycaemia \> administer IV glucose * If glucose status is normal (= no metabolic cause of deterioration) \>\>\> _only & only then_ can do \> CT brain scan _\*\*\* IV artesunate is more preferred than IV quinine as TOC in severe malaria_

Answer 35

**Psychiatric review** As everything is normal \>\>\> Dx goes against HIV Such number of regimen is NOT consistent with current practice \>\>\> Dx goes for factitious So, * Do HIV serology & viral load * Refer to psychiatry for review * A phone to hospital he claimed to be treated at \*\*\* Since O/E and CXR normal \> do NOT indicate CT chest, bronchoscopy, CTPA, AFB, or observation

Answer 36

Indinavir (due to precipitated drug subtance \>\> 10% people who take it have renal stones)

Answer 37

Lamivudine: * Peripheral neuropathy * Skin rash * Arthralgia Co-trimoxazole: * Neutropaenia * Anaemia * Steven-Jhonson syndrome Abacavir: * idiosyncratic hypersensitivity \>\> fever, rash * A/W HLA-B5701 type

Answer 38

Dx: Listeria meningitis + Viral encephalitis * Soft cheese \>\> Listeria monocytogens * Confusion \>\> Viral meningoencephalitis due to HSV, VZV Tx: High dose IV Ampicillin + IV Ceftriaxone + Acyclovir 10-15mg/kg TDS * For Listeria \> Ampicillin (as resistant to cephalosporins) * For HCV/VZV \> Acyclovir * For coverage of other bacteria \> Ceftriaxone

Answer 39

* Co-trimoxazole: As a prophylaxis in HIV & immunosupressed patients * Plecoranil: Antiviral targeting enterovirus * Doxycycline: Lyme meningitis

Answer 40

May/may not mention h/o sexual intercourse: * Hepatitis ( = RUQ pain, deranged LFTs +/- jaundice) * CMV: Acute hepatitis, generalised LNpathy * Close person-to-person contact (including sex) * Incubation 9-90days * Childhood \> Asymptomatic/minimal sign-symptoms * Acute infection \> presents like EBV: fever, malaise, pharyngitis, LNpathy (+/- generalised), splenomegaly +/- hepatitis * In immunocompromised \> life-threatening multi-system disease: retinitis, pneumonitis, colitis * can go through **_unprotected anal sex_** among **_homosexual male_** * Hepatitis C: primary/acute infection is asymptomatic; usually present as chronic hepatitis * HIV seroconversion: 2-12 weeks after infection (usually 2-4weeks, can up to 10months); window period is 4weeks, so HIV test should be positive after 4weeks * **_Hepatitis rules out LGV and Syphilis_** * **_Gonorrhoea may transmit through anal intercourse but \> shows rectal discharge, discomfort (NO hepatitis, NO diarrhoea)_**

Answer 41

Specific site identified (by MRI or other way) * IV Flucloxacillin * It will cover the S. aureus, the most common cause of osteomyelitis * If doesn't work \> test for MRSA \> if +ve, only then offer: Vancomycin + ciprofloxacin * Other options like Co-amoxiclav, Meropenem, Cefotaxime + Metronidazole these can work against S. aureus... can be given if do NOT know the exact site of osteomyelitis * They have S/E of Pseudomonas colitis risk * But when we exact site is known \> Prefer IV flucloxacillin over others (benefit outweigh the risk)

Answer 42

**Await 2weeks of therapy** * Only applicable if - 1. Drug susceptible disease = no signs of drug resistance 2. Do not have clinical or public health need to admit in hospital 3. HIV negative; **(they should be offered HIV test \> if +ve for HIV \> different guidelines)** \*\*\* previous guidlines required "until sputum is -ve for AFB on microcopy", but it updated to **''wait 2 weeks of therapy"** \*\*\* we do not do culture, as it takes minimum 42 days to grow mycobacterium in culture (slow)

Answer 43

* Secondary syphilis \> nephrotic syndrome (acute nephritis: evidence of proteinuria, haematuria) * HBV, HCV \> Mesangiocapillary GN (=membranoproliferative GN) type 1 * HBV \> membranous GN * Plasmodium malariae \> * Membranous GN & Nephrotic syndrome (but NOT acute nephritis) * Immunofluoroscence: granular deposits of IgM, IgG, C3 in mesengial and sub-endothelial areas * Focal segmental glomerulosclerosis (FSGS) * Chronic GN due to this is not reversible by treating the infection alone * Mycoplasma genitalium \> PID *(no renal disease)*

Answer 44

* Arounf 1% will develop fulminant hepatic failure * Acute infectious hepatitis is notifiabel in the UK * In the UK, it is Male \>\>\> Female (may be due to male homosexuality) * 90% of adults will clear the virus completely * 90% of infants will develop persistant disease

Answer 45

* If HIV with CD4 \<100 \> Cryptococcus neoformans \>\>\> TOC: Amphotericin B + Fluocytosine * If NO HIV \> Dx: HSV encephalitis \>\>\> IV Acyclovir * HSV encephalitis will have petechiae in temporal lobe \*\*\* West African + chronic diarrhoea & weight loss for 10 weeks \> episode of shingles 5weeks back + (headache, neck stiffness, increasing confusion) for few days + no mass lesion + 7th nerve palsy + CD4 \<100 + raised ICP (= bilateral papilloedema) \>\>\> Dx: Cryptococcus neoformans \>\>\> TOC: Amphotericin B + Fluocytosine

Pastest: Infectious disease Flashcards

(69 cards)