ID Flashcards
Zika
humans and non-primates are reservoirs
Transmission:
- intrauterine, intrapartum, sex, blood transfusion, lab exposure
Sex: usually male to female.
prolonged viraemia in pregnant women; no evidence of increased susceptibility or severity in pregnant women
Safe sex for 3 months (male) and 2 months (female) after at risk travel
Incubation: 3-14 days (med 5 days)
Sx:
Rash (97%) for 6 days
Pruritis, HA, arthralgia, myalgia, nonpurulent conjunctivitis
fever in 50%
**
Complications:**
- congenital zika syndrome (fetal sequelae worse if infected in first trimester) can occur with both symptomatic and asymptomatic infection
>microcephaly with partial collapsed skull
>thin cerebral cortices with calcifications
>macular scarring and focal retinal mottling
>congenital contracture
>marked early hypertonia and extrapyramidal sx
diagnosis
- nucleic amplification tests (<7days of illness)
any bodily fluid - urine viraemia last longer than blood
- serology after 7 days (may be positive for years) - false negative is possible. can X react with other flaviviruses and vaccines
Symptomatic and pregnant: serum and urine for Zika virus PCR, dengue seum PCR and Dengue IgM
- USS after 4 weeks of infection, then regularly
Zika Virus exposure may breastfeed as transmission through breast milk has not been described although the virus is detectable in breast milk.
Do you add CS for TB meningitis?
YES, lower mortality rate
HIV and TB
Management of treatment-naïve HIV-infected patients with TB is especially challenging in areas with high rates of coinfection. Initiation of antiretroviral therapy (ART) may be complicated by the immune reconstitution inflammatory syndrome (IRIS), which can manifest as reactivation of latent TB, progression of active TB disease, or clinical deterioration in patients previously improving on antituberculous therapy.
For ART-naïve HIV-infected patients with CNS TB, initiation of ART should be delayed for the first eight weeks of antituberculous therapy, regardless of CD4 count. Treat TB first, then start ART after 8 weeks
All HIV-infected patients with TB be treated with ART. The optimal timing depends on the patient’s immune status:
For HIV-infected patients with pulmonary TB and CD4 cell count** <50 cells/microL,** initiation of ART within two weeks after starting TB treatment
For HIV-infected patients with pulmonary TB and CD4 count ≥50 cells/microL, initiation of ART within eight weeks after starting TB treatment
For HIV-infected patients with TB involving the central nervous system (CNS), ART should be delayed for the first eight weeks of antituberculous therapy, regardless of CD4 count.
For HIV-infected patients with baseline CD4 cell count <100 cells/microL on antituberculous therapy and initiating ART within 30 days of starting antituberculous therapy, prophylactic administration of prednisone during the first four weeks following initiation of AR may be considered to reduce the risk of IRIS
Syphilis
What are non-treponemal tests?
RPR and VDRL
Non-specific for syphilis: can be false positive in: pregnancy, SLE, APLS, TB, leprosy, malaria, HIV
**It become negative after treatment **
Syphilis
What are the treponemal specific tests?
realitative only
TP-EIA, TPHA
Syphilis
What do the test results mean?
- Positive non-treponemal test + positive treponemal test —> consistent with active syphilis infection
- Positive non-treponemal test + negative treponemal test–> consistent with a false-positive syphilis result e.g. due to pregnancy or SLE (see list above)
- Negative non-treponemal test + positive treponemal test : consistent with successfully treated syphilis
ESCHAPPM
E: Enterobacter spp.
S: Serratia spp.
C: Citrobacter freundii
H: Hafnia spp.
A: Aeromonas spp.
P: Proteus spp. (P. vulgaris)
P: Providencia spp.
M: Morganella morganii
Inducible beta lactamases
Which ceph has poor cover against gram positive organisms (including strep pneumoniae)?
Ceftazidime
Why ganciclovir in CMV?
Ganciclovir was the first antiviral agent approved for the treatment of cytomegalovirus (CMV) infection. It is widely used for the treatment of CMV infections among patients with impaired cell-mediated immunity, particularly persons with poorly controlled and advanced HIV/AIDS, and recipients of solid organ and bone marrow transplantation, who are at high risk for invasive CMV disease.
The drug is converted intracellularly to ganciclovir 5’-monophosphate by a viral kinase, which is encoded by the cytomegalovirus (CMV) gene UL97 during infection. Subsequently, cellular kinases catalyze the formation of ganciclovir diphosphate and ganciclovir triphosphate, which is present in 10-fold greater concentrations in CMV or herpes simplex virus (HSV)-infected cells than uninfected cells.
Unlike acyclovir, ganciclovir has poor bioavailability (6%) and is therefore given intravenously
What are the main side effects of colistin?
Neuro and nephro toxicity
bacteriocidal abx
causes disruption to outer cell mb
Indications for surgery for native valve endocarditis?
- valve dysfunction causing HF
- Paravalvular extension - abscess, fistula, heart block
- difficult to treat pathogen
- Persistent infection >7days
- Reccurent emboli and elarging vegetations
- mobile vegetation >10mmon the MV or AV with one or more other relative indications
Can PJP be cultured?
no, but the organism needs to be visualised - this can be done with immunofluorescence
Can PJP be cultured?
no, but the organism needs to be visualised - this can be done with immunofluorescence
Why is valacyclovir better than acyclovir?
- faster resolution of acute neuritis
- lower rates of post hepatic neuralgia
Which antifungal or antibacterial medication causes blue-green visual aura?
Voriconazole
Side effects of voriconazole?
- visual changes
- hallucinations
- prolonged QTc
- neuropathy
- CNS alterations - memory, concentration
- alopecia
- photosensitivity rash (linked to SqCC)
Valacyclovir and acyclovir
- Valacyclovir acts as a prodrug for acyclovir
0 Are phosphorylated by virally-encoded thymidine kinase and subsequently by cellular enzymes, yielding acyclovir triphosphate - Acyclovir triphosphate competitively inhibits viral DNA polymerase
Penicillin allergy and other beta lactams
There is approximately two percent cross reactivity between penicillin and cephalosporins. There is approximately 1% cross reactivity between penicillin and carbapenem. There is no cross reactivity between penicillin and monobactams therefore aztreonam is the most appropriate response.
The most frequent causes of brain abscess are Streptococcus and Staphylococcus spp; among these species, viridans streptococci and Staphylococcus aureus are the most common
Paranasal sinuses – Streptococcus spp (especially S. milleri), Haemophilus spp, Bacteroides spp, Fusobacterium spp
●Odontogenic sources – Streptococcus spp, Bacteroides spp, Prevotella spp, Fusobacterium spp, Haemophilus spp
●Otogenic sources – Enterobacteriaceae, Streptococcus spp, Pseudomonas aeruginosa, Bacteroides spp
●Lungs – Streptococcus spp, Fusobacterium spp, Actinomyces spp
●Urinary tract – Pseudomonas aeruginosa, Enterobacter spp
●Penetrating head trauma – Staphylococcus aureus, Enterobacter spp, Clostridium spp
●Neurosurgical procedures – Staphylococcus spp, Streptococcus spp, Pseudomonas aeruginosa, Enterobacter spp
●Endocarditis – Viridans streptococci, S. aureus
●Congenital cardiac malformations (especially right-to-left shunts) – Streptococcus spp
Paradoxical reaction to anti-TB medications
- enlargement of LN size
- occurs in about 20% of pts
- usually occurs between 3 weeks to 4 months
- Culture negative
- ## Male gender is predictive
MOA of antifungals in general
Azole: inhibits Ianosterol 14-a demethylase (CYP450), which converts Ianosterol to ergosterol –> damage to cell mb –> death
Amphotericin: binds to ergosterol and forms pores
Echinocandins: inhibits the enzyme that generates beta glucans
Flucytosine: inhibits DNA synthesis
Donovan bodies
Granuloma inguinale
Mechanism of acyclovir resistance?
●Reduced or absent thymidine kinase
●Altered thymidine kinase activity resulting in decreased acyclovir phosphorylation
●Altered viral DNA polymerase with decreased affinity for acyclovir triphosphate
Quantiferon gold sensitivity and specificity
Sensitivity ~80%
Specificity 98% in low TB pop with no RF
it may stay positive after successful TB treatment therefore cannot be used to assess outcome of treatment.
Antibiotics that have low association with developing C.diff colitis
Aminoglycosides, metronidazole, tetracyclines, teicoplanin, rifampicin and carbapenems
oral ACT (Artemether and lumefantrine combination therapy) absorption is determined by…
presence of rich, fatty food
EBV serology
- IgM and IgG antibodies directed against the Epstein-Barr viral capsid antigen (VCA) are usually present at the onset of clinical illness because of the long viral incubation period.
- IgM levels wane approximately three months later; thus, they are a reliable marker of acute infection in a clinically appropriate picture.
-IgG VCA antibodies persist for life and are a marker of EBV infection.
- IgG antibodies to EBV nuclear antigen (EBNA; a protein expressed only when the virus begins to establish latency) **begin to appear 6 to 12 weeks after the onset of symptoms **and persist throughout life. Their presence early in the course of an illness effectively excludes acute EBV infection.
Which CD4 count do you worry about toxo?
<100
What is the mechanism of fluoroquinolone resistance?
reduced permeability via cell wall
Drug reaction groups
Type A: can affect any individual and are predictable from the known pharmacologic properties of the drug
- make up 90% of all ADR
- i.e. diarrhoea from abx, gastritis from NSAID, aminoglycoside nephrotoxicity
Type B: Occue in susceptible patients, and cannot predict from pharmacologic properties of the drug
- less common 10%
- majority of hypersensitivity reactions mediated by immunological or inflammatory mechanism
- *In addition, there are reactions, referred to as idiosyncratic drug reactions and exaggerated sensitivity reactions, which present with symptoms that do not involve the immune system or inflammatory cells.
TB reactivation
High RF:
- AIDS
- HIV
- Transplantation
- Silicosis
- CKD on RRT
- Carcinoma of head/neck
- Recent TB <2yrs
- abnormal CXR with apical fibronodular changes
- TNF alpha inhibitors
Moderate RF:
- Treatment with GC
- DM
- Young age when infected <4y
What’s different about ertapenam compared to other carbapenem
Narrower spectrum
Active against enterobacteriaceae, and anaerobes
Less active against: pseudomonas, acinetobacter, Gram positive (particularly enterococci and penicillin resistant pneumococci)
The major benefit of ertapenem over other carbapenems is that it has a long half-life and can be administered once daily.
Which antibiotics are NDM1 strain susceptible to?
Colistin, Tigecycline
Clostridium Difficile
- Toxin B is essential for the virulence of C. difficile and is more than 10 times more potent than toxin A on a molar basis for mediating colonic mucosal damage. Thus, strains lacking toxin A can be as virulent as strains with both toxins
- NAP1/BI/027 are hypervirulent strains
- bezlotoxumab (monoclonal antibody against toxin B) together with standard oral antibiotic therapy was associated with a lower rate of recurrent infection than oral antibiotic therapy alone
Botulism
-acute onset of bilateral cranial neuropathies associated with symmetric descending weakness
- Other key features include absence of fever, maintenance of alertness, and lack of sensory deficits other than blurred vision.
- The diagnosis of botulism is confirmed by identification of toxin in serum, stool, vomitus, or food sources or by isolation of C. botulinum from stool, wound specimens, or food sources. However, initial detection of toxin requires one to four days and anaerobic cultures often take up to six days for growth and identification of the organism. Because these confirmatory tests do not yield timely results, the decision to administer antitoxin should be based on the presumptive clinical diagnosis of botulism and not be delayed while awaiting results of confirmatory diagnostic studies. (
Which medications are not used in MDR-TB treatmetn
Rifampicin
Isoniazid
Rifabutin
Thiacetazone
Augmentin
Macrolides
What si the hallmark feature of diffuse scleroderma?
Tendon friction rubs
When to use steroids with PJP tx
CS within 72hr of anti PJP treatement helps to prevent respiratory failure and death in AIDS patients.
All patients with A-a gradient >45 or PaO2 <70 should receive corticosteroids when antimicrobial therapy is initiated.
Treatment for MAC
Clarithromycin or Azithromycin + Ethambutol +/- Rifabutin or Rifampicin
Penicillin is not effective
Tropic diseases with incubation <10d
Dengue
Yellow fever
Zika
Chikungunya
Infuenca
Enteric infections
Rickettsial infection
Tropical disease with incubation period 10-21
Malaria
Thyphoid
Leptospirosis
Brucellosis
Incubation period >21days in tropical disease
Hep A/B/E
Schistosomiasis
TB
Leishmaniasis
vivax malaria
Meliodosis
Trypanomiasis
Tropical diseases with fever and rash
Dengue, Chikungunya, Rickesttsial infection, enteric fever, measles, acute HIV infection
Tropical Diseases
Fever and abdominal pain
Enteric fever, Amboebic liver absces
Tropical Diseases
Fever lasting >2 weeks
Malaria, enteric fever, EBV, CMV, toxo, acute HIV, acute schistosomiasis, brucellosis, TB, Q fever, visceral leishmaniasis
Tropical Diseases
Fever ONSET >6weeks of travel
**Plasmodium vivax or ovale **
Acute Hep B,C, E
TB
Amoebic liver abscess
P. falciparum tx:
Central America: Chloroquine
Otherwise: Artemether-Lumafantire or Atovaquone-proguanil
P. Vivax or ovale tx
PNG/Indonesia: Chloroquine resistant, thus tx with Artemether-Lumafantrine, them primaquine
Otherise:
Chloroquine, then Primaquine
For Primaquine need to screen for G6PD activity
Tafenoquine is the new kid on the block - single dose, but need more G6PD activity
P. Knowlesi
Forest area in SE asia
Need PCR
REsponds to chloroquine
Severe malaria
High parasitaemia >10%
End organ dysfunction
Tx. IV artesunate
Malaria inx
Sporozoites to Liver
Thick film: screening
Thin: density and specification
Which species causing malaria has cyclic fever every 48h?
Plasmodium vivax/ovale
Which species causing malaria is associated with nephrotic syndrome?
Plasmodium malariae: cyclical fever every 72 hours
Plasmodium malariae: is associated with nephrotic syndrome.
Can you use ACT in pregnancy?
No
Leishmaniasis
- intracellular protozoa Leishmania
- bites of sandflies - Different forms: Cutaneous, mucocutaneous leishmaniasis and visceral forms are seen
Cutaneous:
- caused by tropica or mexicana
- crusted lesion at the site of bite +/- underlying ulcer
- if caught in South/Central america - it needs treatment due to risk of transformation to mucocutaneous
Mucocutaneous:
- braziliensis
- skin lesions spread to mucosa
Visceral:
-mostly caused by** Leishmania donovani**
- occurs in the Mediterranean, Asia, South America, Africa
Sx:
Fever, sweats, rigors
Grey skin (Kala-azar)
Pancytopenia with hepatosplenomegaly
Need BM for dx
Trypanosomiasis
- African trypanosomiasis (sleeping sickness)
- American trypanosomiasis (Chagas’ disease).
Trypanosomiasis
African trypanosomiasis, or sleeping sickness
- Trypanosoma gambiense in West Africa - Trypanosoma rhodesiense in East Africa.
Both types are spread by the** tsetse fly. **
Trypanosoma rhodesiense tends to follow a more acute course.
Clinical features include:
- Trypanosoma chancre - **painless subcutaneous nodule at site of infection
- intermittent fever** - enlargement of posterior cervical lymph nodes
- later: central nervous system involvement e.g. somnolence, headaches, mood changes, meningoencephalitis
Treatment:
- IV pentamidine or suramin (early)
- later disease or central nervous system involvement: IV melarsoprol
Trypanosomiasis
American trypanosomiasis, or Chagas’ disease,
Trypanosoma cruzi
- The vast majority of patients (95%) are asymptomatic in the acute phase although a **chagoma **(an erythematous nodule at site of infection) and periorbital oedema are sometimes seen.
- Chronic Chagas disease affects heart and GIT
- CM or arrthythmias
- Megaoesophagus/Megacolon
Treatment:
- benznidazole or nifurtimox
**Interesting facts about rabies
RNA rhabdovirus
travels up the nerve axons towards the central nervous system in a retrograde fashion
- hydrophobia: water-provoking muscle spasms
- hypersalivation
- Negri bodies: cytoplasmic inclusion bodies found in infected neurons
Lyme disease
- spirochete bacteria: Borrelia burgdorferi (North America), B. garinii, B. afzelii (Europe and Asia)
- spread by ticks
- needs tick attachment for >36h for infection
Clinical Features:
stage 1 (early localized stage: 7-14 d post-bite):
■ malaise, fatigue, headache, myalgias
■ erythema migrans: expanding, non-pruritic bulls-eye (target) lesions (red with clear centre) at site of tick bite
- typically develops 1-4 weeks after the initial bite but may present sooner
- usually painless, more than 5 cm in diameter and slowlly increases in size
- present in around 80% of patients
Stage 2 (early disseminated stage: weeks post-infection):
■** CNS: **
aseptic meningitis
CN palsies (CN VII palsy)
peripheral neuritis
■ cardiac: heart block or myocarditis
Stage 3: persistent stage - months to years
■ may not have preceding history of early-stage infection
■ MSK: chronic monoarticular or oligoarticular arthritis
■ acrodermatitis chronicum atrophicans (due to B. afzelii)
■ neurologic: encephalopathy, meningitis, neuropathy
LYme disease
Investigations
ELISA:
Ab to Borrelia burgdorferi
Treatment:
- Doxycycline or Amoxicillin or Cefuroxine
- -if you have erythema migrans, start Abx
Ceftriaxone if stage 2-3
Dengue
- Endemic regions: Asia, Central/South America, Africa, Northern Territory Australia
- Aedes aegypti
- endemic during rainy season
Clinical maifestations:
Dengue fever:
- onset is sudden with high fever (may be biphasic, lasts 2-7 days), severe headache (especially in the retro-orbital area), arthralgia, myalgia, anorexia, abdominal discomfort, and sometimes a macular papular rash.
- Flushing, a characteristic feature is commonly observed on the face, neck, and chest.
Dengue haemorrhagic fever:
- usually follows second exposure/infection
- 1. Acute onset of high fever for 2-7 days
- Haemorrhagic menifestation
- Platelet <100
- Haemoconcentration (rising packed cell volume >20%) or other evidence of plasma leakage—for example, ascites, pleural effusions, low level of serum protein/albumin.
*plasma leakage is more specific/common
Dengue
Investigations
- Low platelet counts of <100 × 109/l.
- Leucopenia early in the illness.
- Atypical lymphocytosis (>15%).
- Abnormal coagulation profile (prolonged activated partial thromboplastin time, prothrombin time, raised fibrinogen degradation products).
- Reduced serum complement levels.
Low albumin
abnormal LFTs
Acidosis
RT-PCR is more specific and sensitive and allows for detection of early infection
**Treatment is just supportive **
Schistosomiasis
parasitic **flatworm infection **
S. mansoni, S. japonicum and S. haematobium.
Katayama fever: acute infection
* fever
* urticaria/angioedema
* arthralgia/myalgia
* cough
* diarrhoea
* eosinophilia
Chronic infection:
- Eggs in cluster in bladder causing inflammation
- looks like calcification in bladder
-** Risk of Squamous cell bladder cancer **
Inx:
- schistosome antibodies in asymptomatic pt
- if symptomatic: gold standard is urine or stool microscopy
Tx:
single oral dose of praziquantel
Toxoplasmosis tx:
Co trimoxazole if not cerebral involvement
Cerebral toxoplasmosis accounts for around 50% of cerebral lesions in patients with HIV: CT: usually single or multiple ring-enhancing lesions, mass effect may be seen
management: **pyrimethamine plus sulphadiazine **for at least 6 weeks
Cryptosporidiosis
protozoal cause of diarrhoea
Cryptosporidium hominis and Cryptosporidium parvum
Sx: watery diarrhoea, abdominal cramps, fever (+/- sclerosing cholangitis, pancreatitis)
modified Ziehl-Neelsen stain (acid-fast stain) of the stool may reveal the characteristic red cysts of Cryptosporidium
Tx:
Nitazoxanide
Rifaximin
Strongyloides stercoralis
threadworm - human parasitic nematode worm
- present in soil and gain access to the body by penetrating the skin.
- Features:
- diarrhoea
- abdominal pain/bloating
- papulovesicular lesions where the skin has been penetrated by infective larvae e.g. soles of feet and buttocks
- larva currens: pruritic, linear, urticarial rash
- if the larvae migrate to the lungs a pneumonitis similar to Loeffler’s syndrome may be triggered
Eosinophilia
Treatment:
ivermectin and albendazole are used
Amoebiasis
Entamoeba histolytica
spread by faecal oral route
causes liver and colonic abscess
Long incubation
Dysentery - stool micro shows trophozoites - tx with **metronidazole **
Liver abscess:
most common in liver (hematologic spread); presents with right upper quadrant pain, weight loss, fever, hepatomegaly
for invasive disease or cyst elimination: follow with iodoquinol or paromomycin
