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Differential diagnosis of bacterial meningitis

Cerebrospinal fluid level Normal level Bacterial meningitis viral meningitis Fungal meningitis Tuberculous meningitis Carcinmatous meningitis
D
C
B
A
Cerebrospinal Fluid
Normal Levels Acute Bacterial M. Acute Viral M. TB M. Neuroborreliosis
Cells/ul < 5 In the 1000s In the 100s In the 100s Some 100
Cells Lymph:Monos 7:3 Gran. > Lymph. Lymph. > Gran. Various leukos Lymph. monocytic
Total Protein (mg/dl) 45-60 Typically 100-500 Typically normal Typically 100-200 Typically up to 350
Glucose Ratio (CSF/plasma) Typically > 0.5 < 0.3 > 0.6 < 0.5 Normal
Lactate (mmol/l) < 2.1 > 2.1 < 2.1 > 2.1 -
Others ICP: 6-22 (cm H2O) PCR of HSV-DNA PCR of TBC-DNA IgG/IgM
CSF/Serum Ratio

classification of bacterial meningitis

According to age group
Age group Etiological agent Clinical features
Neonates and infants
  • A
  • B
  • C
Adults
  • A
  • B
  • C
  • D
Elderly
According to severity of the disease
Mild
Moderate
Severe
According to the duration of disease
Acute
Subacute
Chronic
Adenovirus
Cocksackie A virus
Ebstein barr virus
  • Airway obstruction
  • Splenic rupture
  • X-linked lymphoproliferative disease
  • Lymphomatoid granulomatosis
Less common complications
Gonococcus
Diphtheria
Heamophilis influenza
Fusobacterium necrophorum
Parainfluenza virus


Organ System Findings Suggestive of
General Appearance Normal or ill appearing Depends on area involved in infarction
Vital Signs Fever Poor prognosis

May suggest infectious process

Tachycardia (irregularly irregular) Underlying atrial fibrillation
Absent pulse (radial or carotid artery) Atherosclerosis
Tachypnea Congestive heart failure, concomittant lung disease
Skin Pallor Anemia of chronic disease from any inflammatory condition
Anemia of blood loss from inflammatory bowel disease
Cyanosis Embolism
Abnormal bruising or wound infection
Underlying diabetes mellitus
Eyes Visual field defect Infarct involving posterior cerebral circulation
Absent light reflex Cranial nerve involvement
Speckled appearance of iris with ipsilateral pupil

dilatation

Carotid artery occlusion
Arteriolar constriction, arteriovenous nicking, yellow hard exudates,

cotton wool spots

Hypertensive changes on fundoscopy
Macular edema, microhemorrhages Diabetic eye disease
Ears Deafness Brain stem infarction
Neck Carotid bruit Presence of occlusive extracranial disease
Lungs Cough Congestive heart failure, underlying infection
Heart Arrhythmia Atrial fibrillation
Displaced apical impulse Cardiac enlargement
Murmur Underlying valvular disease
Abdomen Abdominal Tenderness Underlying visceral carcinoma
Palpable abdominal mass Inflammatory bowel disease, Behcet's disease
Hematochezia on rectal exam Inflammatory bowel disease
Back Tenderness over lumbosacaral spine Ankylosing spondylitis
Decreased range of motion of spine Ankylosing spondylitis
Genitourinary Urinary incontinence Anterior circulation stroke
Genital warts Syphilitis uveitis
Genital vesicular lesions Herpitic uveitis
Extremities Joint stiffness and swelling Seronegative spondyloarthropathies, HLA-B27 related uveitis, Reiter's syndrome
Neurological Dysarthria Syphilis, multiple sclerosis
Muscle weakness
Vertigo, deafness, nystagmus and hamiparesis Posterior circulation stroke
Gait abnormalities/Ataxia Cerebellar stroke
Cranial nerve abnormalities Brain stem infarct
Organ System Findings Suggestive of
General Appearance Cachexia Underlying carcinoma
Confused or disoriented Extensive neurological deficit
Vital Signs Fever May suggest concomittant infectious process
Tachycardia (irregularly irregular) Underlying atrial fibrillation
Absent pulse (radial or carotid artery) Atherosclerosis
Tachypnea Congestive heart failure, concomittant lung disease
Skin Pallor Anemia of chronic disease from any inflammatory condition
Abnormal bruising Underlying coagulation disorder
Cyanosis Embolism
Wound infection
Diabetes mellitus
Migratory thrombophlebitis Underlying visceral carcinoma
Eyes Visual field defect Infarct involving posterior cerebral circulation
Absent light reflex Cranial nerve involvement
Speckled appearance of iris with ipsilateral pupil dilatation Carotid artery occlusion
Arteriolar constriction, arteriovenous nicking, yellow hard exudates, Hypertensive changes on fundoscopy
Macular edema, microhemorrhages Diabetic eye disease
Ears Deafness Brain stem infarction
Neck Carotid bruit Presence of occlusive extracranial disease
Lungs Cough Congestive heart failure, underlying infection
Heart Arrhythmia Atrial fibrillation
Displaced apical impulse Cardiac enlargement
Murmur Underlying valvular disease
Abdomen Abdominal Tenderness Underlying visceral carcinoma
Palpable abdominal mass Underlying visceral carcinoma
Genitourinary Urinary incontinence Anterior circulation stroke
Erectile dysfunction Anterior, middle or posterior cerebral infarction
Extremities Cyanosis Embolism
Neurological Dysarthria Suggestive of stroke
Muscle weakness Suggestive of stroke
Vertigo, deafness, nystagmus and hamiparesis Posterior circulation stroke
Gait abnormalities/Ataxia Cerebellar stroke
Cranial nerve abnormalities Brain stem infarct









 
 
 
 
 
 
 
 
 
 
 
 
Airway

Breathing

Circulation
 
AO2
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Early Diagnosis
 
History and PE
Initial diagnostic tests
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Early assessment of ischemic stroke
 
 
 
 
Treatment plan
 
CO3
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Treatment of complications
 
DO2
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Prognosis
 
EO2
 
 
 
 
 
 


Cause of ischemic stroke Revascularization Multifactorial risk reduction
Carotid endartectomy Carotid stenting Antiplatelet therapy Statins Antihypertensives Anticoagulants
Large artery disease Carotid Artery Stenosis g g ++ + + +
Carotid occlusion g g ++ + ++ +
Vertebral artery g g ++ + ++ +
Large vessel atherosclerosis g g ++ + ++ +
Arterial dissection g g ++ + ++ +
Cardiac embolism Atrial fibrillation g ++ + ++ + +
Valvular heart disease ++ + ++ + ++ +
Recent MI ++ + ++ + ++ +
Heart failure ++ + ++ + ++ +
Dilated cardiomyopathy ++ + ++ + ++ +
Hypercoaguable states Protein C/S deficiency ++ + ++ + ++ +
Sickle cell disease ++ + ++ + ++ +
Antithrombin III deficiency ++ + ++ + ++ +

Prevention of stroke can work at various levels including:

  1. primary prevention - the reduction of risk factors across the board, by public health measures such as reducing smoking and the other behaviours that increase risk;
  2. secondary prevention - actions taken to redrombuce the risk in those who already have disease or risk factors that may have been identified through screening; and
  3. tertiary prevention - actions taken to reduce the risk of complications (including further strokes) in people who have already had a stroke.

The most important modifiable risk factors for stroke are hypertension, heart disease, diabetes, and cigarette smoking. Other risks include heavy alcohol consumption (see Alcohol consumption and health), high blood cholesterol levels, illicit drug use, and genetic or congenital conditions. Family members may have a genetic tendency for stroke or share a lifestyle that contributes to stroke. Higher levels of Von Willebrand factor are more common amongst people who have had ischemic stroke for the first time.[1] The results of this study found that the only significant genetic factor was the person's blood type. Having had a stroke in the past greatly increases one's risk of future strokes.

One of the most significant stroke risk factors is advanced age. 95% of strokes occur in people age 45 and older, and two-thirds of strokes occur in those over the age of 65.[2] A person's risk of dying if he or she does have a stroke also increases with age. However, stroke can occur at any age, including in fetuses.

Sickle cell anemia, which can cause blood cells to clump up and block blood vessels, also increases stroke risk. Stroke is the second leading killer of people under 20 who suffer from sickle-cell anemia.[2]

Men are 1.25 times more likely to suffer strokes than women,[2] yet 60% of deaths from stroke occur in women. Since women live longer, they are older on average when they have their strokes and thus more often killed (NIMH 2002).[2] Some risk factors for stroke apply only to women. Primary among these are pregnancy, childbirth, menopause and the treatment thereof (HRT).

Prevention is an important public health concern. Identification of patients with treatable risk factors for stroke is paramount. Treatment of risk factors in patients who have already had strokes (secondary prevention) is also very important as they are at high risk of subsequent events compared with those who have never had a stroke. Medication or drug therapy is the most common method of stroke prevention. Aspirin (usually at a low dose of 75 mg) is recommended for the primary and secondary prevention of stroke. Also see Antiplatelet drug treatment. Treating hypertension, diabetes mellitus, smoking cessation, control of hypercholesterolemia, physical exercise, and avoidance of illicit drugs and excessive alcohol consumption are all recommended ways of reducing the risk of stroke.[3]

In patients who have strokes due to abnormalities of the heart, such as atrial fibrillation, anticoagulation with medications such as warfarin is often necessary for stroke prevention.[4]

Procedures such as carotid endarterectomy or carotid angioplasty can be used to remove significant atherosclerotic narrowing (stenosis) of the carotid artery, which supplies blood to the brain. These procedures have been shown to prevent stroke in certain patients, especially where carotid stenosis leads to ischemic events such as transient ischemic attack. (The value and role of carotid artery ultrasound scanning in screening has yet to be established.)

A meta-analysis concluded that lowering homocysteine with folic acid and other supplements may reduce stroke.[5] However, the two largest randomized controlled trials included in the meta-analysis had conflicting results. Lonn reported positve results;[6] whereas the trial by Toole was negative.[7]



Vessel involved Physical examination
Anterior cerebral artery [8][9]
  • Decreased motor strength- contralateral lower limb[8]
  • Absent or decreased sensations-contralateral lower limb[8]
  • Increased reflexes-contralateral lower limb
  • Babinski's reflex positive
  • Hemineglect [9][10]
  • Transcortical motor aphasia(non fluent)[9][10]
  • Mutism
  • Contralateral grasp and sucking reflex
  • Memory impairment[11]
  • Confabulation[12]
  • Hypersexual gestures
Middle cerebral artery[13]
  • Most common site of infarction
Posterior cerebral artery[20][21][22][23][22][24]
Vertebrobasilar artery[28] Midbrain-Weber syndrome[29]
  • Contralateral decreased motor strength
  • Ipsilateral 3rd nerve palsy
Medulla
  • Ipsilateral Xth cranial nerve palsy
  • Horner's syndrome
  • Impaired pain, touch and temperature sensation on the upper half of the face
  • Romberg's sign
  • 12th cranial nerve palsy
  • Contralateral decreased motor strength
  • Contralateral loss of position sense, vibration and two point discrimination
Pons

Locked-in syndrome [34][35]

Cerebellum


Stroke

Aysha's sandbox

TOAST CLASSIFICATION OF Acute ISCHEMIC STROKE:

  • Large artery atherosclerosis
  • Cardioembolism
  • Small vessel occlusion-Lacunar infarct
  • Stroke of other, unusual, determined etiology
  • Stroke of undetermined etiology

Based on duration of symptoms:

  • Transient ischemic stroke
  • Acute ischemic stroke
  Most common
  • Chronic ischemic stroke:
   Uncommon

Ischemic stroke due to cause:

  • Artherosclerotic
  • Non Artherosclerotic
  • Systemic hypoperfusion
   Heart failure
    Blood loss
    Low BP


PATHOPHYSIOLOGY: Hemodynamic changes:

  • Reduction in blood flow due to systemic hypoperfsuion, involves watershed areas

hippocampal pyramidal cells, cerebellar Purkinje cells, and cortical laminar cells

  • Thrombosis acutely or chronically, involves extrascranail and intracranial vesssels. Atherosclerotic blood vessels , plts adhere to plaque causing occlusion
  • Embolic stroke: clot foms elsewhere in the body and travels to the brain, usually heart in afib, other emboli causing stroke involves tumour, septic embolus, venous clot or fat
  • Embolic stroke-cortical undergo hemorrhagic transformation
  • Lacunar infarction: involves small penetrating vessels, chronic hypertension causes thickening of media and fibrinoid depositon in the vessel wall causing lumen narrowing and occlusion.

Ususally subcortical but any site can be involved. Non atherosclerotic causes such as

               *Arterial dissection 

•Fibromuscular dysplasia •Vasculitis •Moyamoya disease •Sickle cell disease arteriopathy •Focal cerebral arteriopathy of childhood

Cause Pathogenesis area involved

Cellular changes:

  • Focal ischemia-area affected by single blood vessel and its surrounding branches. Central core of tissue die by necrosis as directly supplied by the blood vessel, called infarct.

The cells surrounding the central infarct supplied by collateral vessels receive some oxygen and glucose, at increased risk of infarction but can be salvaged by increase in blood flow to the area called Pneumbra. Molecular changes:

  • Depletion of ATP
  • Acidosis, lactate increased
  • Ionic imbalance: Na,K, Ca
  • Increase in excitatory neurotrasmittor glutamate at synases due to neuronal electrical failure-

Glutamate receptor stimulation NMDA receptors –opening of ion channels, increased calcium and sodium influx and potassium eflux

  • Increased Na influx and water-edema and causes decreased uptake of glutamate resulting in excitotoxicity state in the brain
  • NMDA receptor activation causes increase NO levels in the brain-excessive levels acts as a free radical-reacts with other free oxygen radicals producing peroxynitirite causing breaks in DNA and DNA damage- Apoptosis

Type of cell death after ischemia Type of infarct time of initiation of cell death Main mechanism of cell death Area invol

  • Global ischemia delayed after 12 hours –several days Apoptosis Hippoca
                                                                                                                                        Striatum
                                                                                                                                 2 and 5 cort la
  • Focal ischemia Within 3-4 hours -12 to 24hrs Necrosis central core by necrosis and periphery by apoptosis centre

Loss of brain structural integrity Cerebral edema: Vasogenic: Disruption of bbb Celluar/cytotoxic: ATP dep ion regualtion disrupted Cerebral autoregulation

Cerebral blood flow determinants

*resistance of cerebral blood vessel 
  • Cerebral perfusion pressure
  • Cerebral blood flow is maintained in the pressure range of 60-150 mmg
  • Cerebral blood flow increases in cases of low pressure by vasodilation- nitric oxide release by endothelial cells
  • Blood flow decreases by vasoconstriction at high pressures. Smooth muscles in the Bv are the sensors for detection of blood vessels

Pressure below 60 mmhg ischemia Pressure above 150 mmhg edema

Cerebral autoregulation failure during ischemia: Low pressures- cerebral vasodilation to increase blood flow-increased oxygen extraction ratio initially to maintain oxygen levels in the brain cells-further dcline in blood presssure- compensatory mechanisms fail-inhibtion of protein synthesis 35ml/100gm/min, increased glucose utilization – 25ml/100gm/minanaerobic glycolysis-tissue acidosis-neuronal electric failure16-18ml/100gm/min-cell membrane dysfunctionml/100gm /min 10-12-cell death (infart) In hypertension autoregulation set at higher pressures so drop to normal levels may exacerbate ischemia GENETICS:

PITX2 and ZFHX3 for cardioembolic stroke

•HDAC9 for large vessel disease •ABO for all ischemic stroke

Cause of ischemic stroke Revascularisation
A B
A B
A A
A A





D
C
B
A
Cause of ischemic stroke Revascularisation Multifacrorial risk reduction
D
C
B
A
 
 
 
 
 
 
 
Ischemic stroke
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Based on duration of symptoms
 
 
 
 
 
 
 
 
Based on cause)
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
TIA
 
Acute Ischemic stroke
 
 
 
 
 
abc
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 





Cause of ischemic stroke Revascularisation Multifactorial risk factor reduction
Carotid endartectomy Carotid stenting ++ + ++ +
a a a ++ + ++ +
b b ++ + ++ +
C c c ++ + ++ +
d d d ± ++ ± ++

Prognosis of ischemic stroke 1)a)age, stroke severity, stroke mechanism, infarct location, comorbid conditions, clinical findings, and related complication; b) interventions such as thrombolysis, stroke unit care, and rehabilitation can play a major role in the outcome of ischemic strok c)acute phase of stroke, the strongest predictors of outcome are stroke severity and patient age. 2):Bruno A, Biller J, Adams HP Jr, Clarke WR, Woolson RF, Williams LS, et al. Acute blood glucose level and outcome from ischemic stroke.aird TA, Parsons MW, Phanh T, Butcher KS, Desmond PM, Tress BM, et al. Persistent poststroke hyperglycemia is independently associated with infarct expansion and worse clinical outcomeMandelzweig L, Goldbourt U, Boyko V, Tanne D. Perceptual, social, and behavioral factors associated with delays in seeking medical care in patients with symptoms of acute strokeTissue plasminogen activator for acute ischemic stroke. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study GroupAcute stroke: usefulness of early CT findings before thrombolytic therapy

3)Poor prognostic factors: Severe middle cerebral artery infarction

  • Large area of brain involvement
  • Other co morbid conditons
  • Advanced age
  • Severe hemiplegia

4)Good prognostic factors: 5)NIHSS score predicts early mortality predicts prognosis; The NIHSS score strongly predicts the likelihood of a patient's recovery after stroke. A score of > or =16 forecasts a high probability of death or severe disability whereas a score of < or =6 forecasts a good recovery. 6)The 1-year mortality in first-time stroke sufferers is 14% to 24% in persons aged 40 to 69 years, and the 1-year mortality increases to 22% to 27% in patients aged 70 years and older. (Find citation)


CDC Stroke kills almost 130,000 Americans each year—that’s 1 out of every 20 deaths.1 On average, one American dies from stroke every 4 minutes.2 Every year, more than 795,000 people in the United States have a stroke. About 610,000 of these are first or new strokes. About 185,00 strokes—nearly one of four—are in people who have had a previous stroke.2 About 87% of all strokes are ischemic strokes, when blood flow to the brain is blocked.2 Stroke costs the United States an estimated $34 billion each year.2 This total includes the cost of health care services, medications to treat stroke, and missed days of work. Stroke is a leading cause of serious long-term disability.2 Classification of Ischemic Stroke: According to the causative agent:

  • Thrombotic
  • Embolic
  • Small vessel disease
  • Systemic hypoperfusion
  • Crytogenic-Undetermined etiology

Toast classification of ischemic stroke: According to anatomical location:

  • Cortical
frontal, parietal, temporal and occipital lobes
disrupt higher cognitive function. 
  • Subcortical
internal capsule, thalamus, basal ganglia, brainstem and cerebellum. 
  • Watershed areas

According to vessel involved:

  • Anterial cerebral artery
  • Middle cerebral artery
  • Posterior cerebral artery

According to duration of symptoms:

  • Acute
  • subacute
  • Chronic

According to clinical presentaion

  • Pure Motor
  • Pure Sensory
  • Mixed



Class I
"1."(Level of Evidence: ) "
"2."(Level of Evidence: ) "
Class IIa
"1."(Level of Evidence: ) "
Class IIb
"1."(Level of Evidence:) "
"2."(Level of Evidence:) "

Stroke epidemiology PMID: 26673558 In 2013, stroke fell from the fourth to the fifth leading cause of death in the United States, behind diseases of the heart, cancer, chronic lower respiratory diseases, and unintentional injury. ●● From 2003 to 2013, the relative rate of stroke death fell by 33.7% and the actual number of stroke deaths declined by 18.2%. Yet each year, ≈795 000 people continue to experience a new or recurrent stroke (ischemic or hemorrhagic). Approximately 610 000 of these are first events and 185 000 are recurrent stroke events. In 2013, stroke caused ≈1 of every 20 deaths in the United States. On average, every 40 seconds, someone in the United States has a stroke, and someone dies of one approximately every 4 minutes. ●● The decline in stroke mortality over the past decades, a major improvement in population health observed for both sexes and all race and age groups, has resulted from reduced stroke incidence and lower case fatality rates. The significant improvements in stroke outcomes are concurrent with cardiovascular risk factor control interventions. The hypertension control efforts initiated in the 1970s appear to have had the most substantial influence on the accelerated decline in stroke mortality, with lower blood pressure distributions in the population. Control of diabetes mellitus and high cholesterol and smoking cessation programs, particularly in combination with hypertension treatment, also appear to have contributed to the decline in stroke mortality. ●● Approximately 10% of all strokes occur in people 18 to 50 years of age. Between 1995 and 2008, National Health Interview Survey data reveal that hospitalizations for ischemic stroke increased among adolescents and young adults (aged 5–44 years), whereas subarachnoid hemorrhage hospitalizations decreased during that same time period. ●● Stroke death rates declined more among people aged ≥65 years (−54.1%; from 534.1 to 245.2 per 100 000) than among those aged 45 to 64 years (−53.6%; from 43.5 to 20.2 per 100 000) or those aged 18 to 44 years (−45.9%; from 3.7 to 2.0 per 100 000).


Common complications

Common complications
Duration Complications
Early complications

Suppurative complications

Non suppurative complications

Late complications
Adenovirus
Cocksackie A virus
Ebstein barr virus
  • Airway obstruction
  • Splenic rupture
  • X-linked lymphoproliferative disease
  • Lymphomatoid granulomatosis
Less common complications
Gonococcus
Diphtheria
Heamophilis influenza
Fusobacterium necrophorum
Parainfluenza virus


Pathogen Complications
Diphtheria
  • A
  • B
  • C
  • D
Gonococcus
  • A
  • B
  • C
  • D
'
  • A
  • B
  • C
  • D
Cocksackie A virus
  • A
  • B
  • C
  • D
Ebstein barr virus
  • A
  • B
  • C
  • D
Gonococcus
  • B
  • C
  • D
HIV
  • B
  • C
  • D

MRI syphilis 17628376


Among women the median prevalence of genital warts was 1.1% (range 0.8 to 2.3) across all jurisdictions, compared to 4.0% (range 2.9 to 4.7) for MSM and 4.9% (range 3.3 to 5.5) for MSW.
Varicella containing vaccines Indications Efficacy and immunogenicity Recommended dose Duration
Varicella vaccine (Varivax)
  • Approved for persons 12 months and older
  • Detectable antibody
  • 97% of children 12 months through 12 years following 1 dose
  • 99% of persons 13 years and older after 2 doses
  • 70% to 90% effective against any varicella disease
  • 90%-100% effective against severe varicella disease
  • 2 doses separated by at least 4 weeks
Measles-mumps-rubella-varicella vaccine (ProQuad)
  • Approved for children 12 months through 12 years
  • Do not use for persons 13 years and older
  • Efficacy of MMRV vaccine was inferred from that of MMR vaccine and varicella vaccine on the basis of noninferior immunogenicity
  • Formal studies to evaluate the clinical efficacy of MMRV vaccine have not been performed[36]
  • May be used for both first and second doses of MMR and varicella vaccines
  • Minimum interval between doses is 3 months
Herpes zoster vaccine (Zostavax)
  • Approved for persons 50 years and older
  • Vaccine recipients 60 to 80 years of age had 51% fewer episodes of zoster
  • Efficacy declines with increasing age
  • Significantly reduces the risk of postherpetic neuralgia
  • Reduces the risk of zoster 69.8% in persons 50 through 59 years of age
  • Single dose at age 60 years or older (whether or not they report a prior episode of herpes zoster)
New Herpes zoster vaccine (Shingrix)
  • Adults aged 50 years or older (first pivotal phase 3 trial)
  • Adults aged 70 years and over (second pivotal phase 4 trial)
  • 89% (95% confidence interval: 69– 97) efficacious in preventing PHN in people aged 70 years
  • 91% (95% confidence interval: 76– 98) efficacious in people aged 50 years and over.
  • Two doses

| colspan="3" style="background: #4479BA; text-align: center;" | For individuals with penicillin allergy |- | style="padding: 5px 5px; background: #DCDCDC;" | Cephalexin, oral | style="padding: 5px 5px; background: #F5F5F5;" |

  • 20 mg/kg/dose twice daily (max = 500 mg/dose)

| style="padding: 5px 5px; background: #F5F5F5;" |

  • 10 days

|- | style="padding: 5px 5px; background: #DCDCDC;" | Cefadroxil, oral | style="padding: 5px 5px; background: #F5F5F5;" |

  • 30 mg/kg once daily (max = 1 g)

| style="padding: 5px 5px; background: #F5F5F5;" |

  • 10 days

|- | style="padding: 5px 5px; background: #DCDCDC;" | Clindamycin, oral | style="padding: 5px 5px; background: #F5F5F5;" |

  • 7 mg/kg/dose 3 times daily (max = 300 mg/dose)

| style="padding: 5px 5px; background: #F5F5F5;" |

  • 10 days

|- | style="padding: 5px 5px; background: #DCDCDC;" | Azithromycin, oral | style="padding: 5px 5px; background: #F5F5F5;" |

  • 12 mg/kg once daily (max = 500 mg)

| style="padding: 5px 5px; background: #F5F5F5;" |

  • 5 days

|- | style="padding: 5px 5px; background: #DCDCDC;" | Clarithromycin, oral | style="padding: 5px 5px; background: #F5F5F5;" |

  • 7.5 mg/kg/dose twice daily (max = 250 mg/dose)

| style="padding: 5px 5px; background: #F5F5F5;" |

  • 10 days

|- |}



Transmission Clinical Presentation Disease Diagnosis Mother to Child Transmission Most Serious Complications
Laboratory studies Clinical Diagnosis Vertical Transmission Trans-vaginal transmission
Primarily sexually transmitted Genital Dermatological Manifestation
(e.g., ulcers, chancre, vesicles, warts, balanitis etc.)
HPV Cervical Cancer
Herpes simplex-2 Severe pruritis/discomfort
Syphilis *Neurosyphilis
*Cardiosyphilis
Scabies Moderate to Severe pruritis/discomfort
Pubic lice Moderate to Severe pruritis/discomfort
Candidiasis
(in males)
Mild to moderate pruritis/discomfort
Generalized Symptoms
(e.g. constitutional symptoms
HIV *Primary CNS Lymphoma
*Immunosuppression (AIDS)
Syphilis *Neurosyphilis
*Cardiosyphilis
Urogenital infections
(e.g.,Vaginitis, Urethritis, Cervicitis, and PID)
Gonorrhea PID
Chlamydia PID
Syphilis *Neurosyphilis
*Cardiosyphilis
Mycoplasma genitalium unknown unknown PID
Trichomonas vaginalis PID
Less frequently sexually transmitted Generalized Symptoms
(e.g. constitutional symptoms)
Zika Virus Vertical transmission and Congenital abnormalities
Hepatitis B Hepatocellular Carcinoma
Hepatitis C Liver cirrhosis
Urogenital Infections
(e.g.,Vaginitis, Urethritis, Cervicitis, and PID)
Gardnerella vaginalis Moderate to severe discomfort
Candidiasis
(in females)
Moderate to severe pruritis/discomfort
Ureaplasma urealyticum Moderate to severe pruritis/discomfort

Postexposure prophylaxis

Active immunisation

Varicella vaccine is recommended for immunocompetent individuals exposed to varicella infection but did not receive full two dose course of vaccine previously[37][38]

Passive immunisation

VZV immunoglobulin

  1. Bongers T, de Maat M, van Goor M; et al. (2006). "High von Willebrand factor levels increase the risk of first ischemic stroke: influence of ADAMTS13, inflammation, and genetic variability". Stroke. 37 (11): 2672–7. PMID 16990571.
  2. 2.0 2.1 2.2 2.3 National Institute of Neurological Disorders and Stroke (NINDS) (1999). "Stroke: Hope Through Research". National Institutes of Health.
  3. American Heart Association. (2007). Stroke Risk Factors Americanheart.org. Retrieved on January 22, 2007.
  4. American Heart Association. (2007). Atrial Fibrillation Americanheart.org. Retrieved on January 22, 2007.
  5. Wang X, Qin X, Demirtas H; et al. (2007). "Efficacy of folic acid supplementation in stroke prevention: a meta-analysis". Lancet. 369 (9576): 1876–82. doi:10.1016/S0140-6736(07)60854-X. PMID 17544768.
  6. Lonn E, Yusuf S, Arnold MJ; et al. (2006). "Homocysteine lowering with folic acid and B vitamins in vascular disease". N. Engl. J. Med. 354 (15): 1567–77. doi:10.1056/NEJMoa060900. PMID 16531613.
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