c.

Can be from petting animals then touching mouth

4. Name a species of this viral group that has been eradicated worldwide through vaccination:
a. Poliovirus
5. What samples should be sent to microbiology laboratory for detection of pathogen?
a. Swabs of blister/vesicles and faeces for viral PCR
6. What complications can occur?
a. Herpengina – mouth infection caused by coxsackieviruses
b. Viral meningitis
c. Myocarditis
d. Pericarditis
7. How can we prevent its further spread in the community?
a. Isolation, hand hygiene, respiratory etiquettes, no swimming in beaches
b. Public health notification

HAND, FOOT & MOUTH DISEASE

 Cause: Coxsackie A, B; RNA picornavirus (enterovirus)

 Features: low grade fever, headache, vesicles on hands/feet/mouth (IP: 3-10 days), conjunctivitis, herpengina
o Can be complicated by aseptic meningitis, myo-pericarditis
o Nb: no GI symptoms, despite enterovirus group
 Laboratory samples: swabs (lesions), faeces – viral PCR
 Different from foot & mouth disease in animals – that is from picornavirus (Apthovirus) – usually not transmitted to humans
as likely killed by acid in stomach, quarantine & culling animals
 Management: supportive
 Prevention: isolation, hand hygiene, respiratory etiquettes, no swimming in beaches, PH notification

CASE 6A

A 4-year-old boy presents with recurrent lesions on his upper lip. He has runny nose and eyes and tends to intensely scratch the
lip before the appearance of these lesions. His mother is very anxious as every few months he has to miss the day care due to
these lesions.

1. Describe the rash type:

a. Crops of blisters / papules
b. Golden crusted
2. What is the differential diagnosis?
a. Cold sores (Herpes Simplex Virus, HSV)
b. Impetigo (Staphyloccocus aureus)

The GP takes a swab of the lesion to reassure the mother and send him home on topical application. The
gram stain of the lesion is shown in picture.

3. Describe the organism:

a. Gram-positive cocci in clusters (grape-like) = Staphylococci spp.
4. What would be the right treatment in this case? Why?
a. Ideal treatment: oral flucloxacillin / Erythromycin syrup (in case of penicillin allergy)
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 b. Topical fusidic ointment (discouraged)

IMPETIGO

 Cause: usually due to Staphylococcus aureus

 Features:
o Blister – golden crusted
o Can occur anywhere, most commonly the face
o Very contagious (so no sharing of towels)
 D/D: HSV 1 (primary, reactivation), Strep. Pyogenes
 Management:
o Oral flucloxacillin / erythromycin
o Topical fusidic ointment (discouraged)

CASE 6B

The child comes back in 3 days acutely unwell, hypotensive with generalized rash and shedding sheets of skin. He is transferred to
the paediatric ward, commenced on IV fluids, IV Ceftriaxone and gentamicin.

5. Name the syndrome associated with shedding sheets of skin & sepsis
a. Staphylococcal scalded skin syndrome (SSSS)
6. What could be the underlying pathogenesis?
a. Toxin-mediated
b. Epidermolysis A, B causes SSSS in children & toxic epidermal necrolysis in adults
c. Enterotoxin A, B, C causes toxic shock syndrome (TSS)
7. What is the name of this clinical sign, and what does it elicit?
a. Nikolsky sign – formation of blister upon lateral pressure to the fragile skin

STAPHYLOCOCAL SCALDED SKIN SYNDROME

 Cause: Staph aureus

o Toxin-mediated: epidermolysin A, B (SSSS in children, TEN in adults)
o Enterotoxin A, B, C (TSS)
 Features:
o Sick baby, acute onset
o Generalised rash followed by shedding of skin sheets in 2-5 days
o Nikolsky sign: intraepidermal blister induced with lateral pressure on fragile skin
 Management:
o Emergency admission
o Requires IV antibiotics
o Fluid rehydration

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CASE 7

A 5 y old child presents with a rash, fever and vomiting. He has been suffering from pharyngitis lately. On examination his tongue
looks red.

1. Describe the skin lesion & appearance of the tongue:

a. Generalised maculopapular rash
b. Strawberry tongue
2. What test will you perform to evaluate the rash, and why?
a. Glass test
b. Differentiating between blanching & non-blanching
3. What microbiological specimens would you like to send to the laboratory?
a. Throat swab: bacterial culture & viral PCR
i. Not tongue swab
b. Blood culture
4. Lab technician performs a Gram stain on a pathogen grown from his throat swab. Describe what is seen on the Gram stain:
a. Gram positive cocci in chains – Streptococci

b.
5. Bacterial culture plate in the laboratory shows haemolysis around the bacterial colonies (picture). What could be the reason
for haemolysis and does it have any role in this disease process?
a. Group A beta-haemolytic Streptococcus produces erythrogenic exotoxin that breaks down RBCs in the culture media
around the bacterial growth
b. This is the virulence factor in the causation of this disease

6. What is your final diagnosis?

a. Scarlet fever – caused by Group A Streptococcal bacteria
7. How will you treat this child?
a. Oral penicillin V for 7-10 days
8. What complications can occur with this infection?
a. Suppurative (pus): otitis media, sinusitis, tonsillar abscess, bacteraemia
b. Non-suppurative, immunologically-mediated: rheumatic fever, glomerulonephritis
9. Is it a notifiable disease?
a. Yes
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SCARLET FEVER

 Notifiable disease!
 Cause: Group A beta-haemolytic Streptococcus
o Erythrogenic exotoxin mediated
o ASO titre raised - Antistreptolysin O, measuring AB’s against streptolysin O (produced by Group A strep bacteria)
 Features:
o <10 years age
o Incubation 2-4 days
o Bright red blanching rash (sandpaper)
 First in axillae/groins, then widespread
o Red face with circumoral (around the mouth) pallor
o Strawberry tongue
o Fever, headache, vomiting
 Treatment:
o Symptomatic relief
o Penicillin V, 7-10 days
 Complications:
o Suppurative: otitis media, sinusitis, tonsillar abscess, bacteraemia
o Non-suppurative: rheumatic fever, glomerulonephritis

CASE 8

A 17 year old presents to paediatric outpatients with fever, dysuria and increased urinary frequency. Urine is sent for laboratory
examination. The patient informs the doctor that she is allergic to penicillin/cephalosporins and nitrofurantoin. The doctor
prescribes her cotrimoxazole (trimethoprim + sulfamethaxazole) for 5 days with plenty of fluids.

One week later, the patient presents (see picture) with a blood pressure of 80/60 mm Hg. She is admitted to the intensive care.

1. Describe lesions in the picture:

a. Macules, purpura, swollen lips
2. State your hypothesis (pathogenesis) for these changes:
a. Allergic reaction to one of the above drugs? Sulfa (sulphonamide) component in contrimoxazole
3. What is the disease, and at what stage is it?
a. Toxic Epidermal Necrolysis (TEN)
4. The doctor takes a detailed history and orders various blood tests. WBC count is 15, 500 cells/mm (Ref range: 4,000-11,000
cells/cm2) with peripheral blood smear as shown. What does the WBC count indicate?
a. Leukocytosis-raised WBC

5. What does the peripheral blood smear show?

a. Eosinophilia (raised eosinophil count – pink granulated cytoplasmic cells)
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6. Skin biopsy shows as follows. What pathology can you seen in the skin biopsy?

a.
b. Epidermal necrolysis: normal keratinocytes, colloid bodies, lymphocytes in dermis, vacuolated basal epidermal cells
7. How would you manage this patient?
a. Stop Cotrimoxazole
b. Support ABC (airway/breathing/circulation)
c. Steroids as an anti-immune agent
d. Eye drops to keep eyes moist

STEVENS JOHNSON SYNDROME

 Classification

o
 Aetiology:
o Drugs causing Stevens-Johnson syndrome – PCP LAPSE
o Phenytoin
o Carbamazepine
o Phenobarbital
o Lamotrigine
o Allopurinol
o Penicillin
o Sulfa drugs
o Erythromycin
 Complications: ocular, septicaemia, secondary infection, pneumonitis, acute renal failure, UTI, congestive cardiac failure,
pulmonary oedema, metabolic encephalopathy, hepatic encephalopathy, intracranial bleed

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LC: EPIDEMICS, AND HOW TO CONTROL THEM

EPIDEMICS IN THE PAST

 Leprosy, plague, typhus, trachoma, small pox, influenza (English Sweating Disease), erysipelas
 Scurvy, ergotism, lead poisoning, plica polonica – you don’t need to have an infectious cause for an epidemic

BUBONIC PLAGUE

 Yersinia pestis from fleas on rats

o The fleas transmits bacterium from household to household
 Swollen gland (“buboes”); fever, chills, headache
 Extreme exhaustion
 Mortality 30%

SARS – SEVERE ACUTE RESPIRATORY SYNDROME

 New coronavirus – arose in HK

 ASEAN countries estimated to have lost $25 billion USD in 2003; 1% reduction in Toronto’s $200 billion USD economy

MERS-COV

 Middle East Respiratory Syndrome

 New coronavirus – arose in Saudi Arabia
 Respiratory symptoms (cough, shortness of breath SoB)
o +/- pneumonia
o +/- GI symptoms
 40% mortality
 Camel reservoir?

EBOLA VIRUS

 3 West African countries: Guinea, Liberia, Sierra Leone

 In June 2014: 750 infected; 500 died
o In February 2015: 22,300 infected; 8,900 died
 Fruit bats – natural host of the virus
 Symptoms – high fever, bleeding, CNS damage
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 Fatality rate ~50%
 Incubation period – 2-21 days
 No vaccine / cure
 Supportive care = rehydration for diarrhoea & vomiting

ZIKA VIRUS

 Causes: flavivirus (includes dengue & yellow fever virus)

o Microcephaly in-utero
o Neurological problems (Guillain Barré)
 Symptoms: rash, fever, conjunctivitis, headache, malaise, arthralgia
 Incubuation – around a few days?
 Diagnosis: symptoms
 Rx: rest, analgesics (mild Rx)
 Public health: Aedes aegypti vector; human to human / sexual contact?

INFLUENZA

 Excess mortality in 1918 influenza pandemic

 Timeline of Influenza A serotype emergence:

o Each point indicates a distinct avian influenza serotype known to have caused human infection
 Triangle = avian host; cross = swine host; circle = no identified animal host

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 Can see the difference between “drift” and “shift”
 Influenza H5N1 virus:
o Causes severe disease in chickens & humans
 Pneumonia
 Severe systemic infection
 Diarrhoea
 Encephalitis
 Death

MATHS

 R0 = reproduction number
o Number each infected individual will infect in a population that has no immunity to the disease
 S = susceptibility (0-1)
o Proportion of the population susceptible to the disease (i.e. not immune) (0 – 100%)

STEADY STATE

 Endemic, where R0 = 1
o On average, each infected person infects one other person
o R0 x S = 1
 Each infected person infects one other person
 So what happens when…
o R0 x S < 1
 Disease will eventually die out, as it is infecting less than one person
o R0 x S > 1
 Epidemic – geometrical progression

HOW CAN WE CONTAIN PANDEMICS?

 Containment = elimination of virus before spread is extensive

o I.e. going from ‘R0 x S > 1’ to R0 x S < 1’
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WHAT ARE THE OPTIONS?

 Quarantine cases + contacts

 International travel restrictions
 Vectors
 Travel restriction within country
 Vaccine (especially early cases)
 School / university closures
 Cancel mass gatherings
 Personal hygiene measures
 Use of masks by general public

CONTROL

 Quarantine “40 days” for shipping

 Vaccination
 Vector control – plague, malaria
o Methods to eliminate or eradicate any animal that carries & transmits pathogens (vectors)
 Fomites – any object or material, which are likely to carry infection from one individual to another

MASS GATHERINGS

 Obvious target
 Significant source of community transmission ?
 Evidence

PERSONAL HYGIENE

 Respiratory hygiene
 Handwashing

SMALLPOX, VARIOLA

 Eradiation worldwide in 1979

o Only infection in the world that we have been able to remove
 Vaccine history important here – Dr Edward Jenner connecting milkmaid’s cowpox immunity and lack of smallpox

POLIO

 Scourge of polio
 “Infantile paralysis”
 Vaccines: 1955 Salk, 1961 Sabin
 Almost eradicated
 1955 disaster in the USA
o Wild virus included in the vaccine of 120,000 doses
o 56 children developed polio, 5 children died

MEASLES

 Acute respiratory infection

 Rash
 Complications:

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 o Hospital admission 1:4
o Middle ear infection 1:10
o Pneumonia 1:20
o Brain damage (subacute sclerosing pan-encephalitis) 1:1,000
o Death: 1:1,000

HERD IMMUNITY

 Protecting everyone by achieving low rate of S (susceptibility)

o R0 x S < 1
 S reduced by:
o Vaccination
o Quarantine
o Vector control
o Fomite control
 S = mean age of being infected ÷ mean age of death (any cause)

FREE RIDING

 Herd immunity protects even the un-vaccinated

o Diseases die out, protecting everyone by achieving low rate of S

ADVERSE PUBLICITY WITH MMR VACCINE

 Andrew Wakefield: speculative conclusion of MMR vaccine causing autism

o Charged with fraud & deregistered
 MMR uptake after age 2 years, by deprivation category, birth cohorts, 1988-2000


 8x fold in number of districts with >20% susceptibility

INCENTIVES

 Childcare vaccination legislation – ECEC services can choose to refuse enrolment or attendance of children whose
immunisation is not up to date (but does not make immunisation mandatory)
 Centrelink payments can only be paid for children who meet immunisation requirements

INFLUENZA-LIKE-ILLNESSES (ILI)

 We get ILI per year – less than one is true influenza

EFFICACY OF INLUENZA VACCINE IN HEALTHY ADULTS

 Harms:
o Injection site – red, sore/tender
o Rare events – Guillan-Barré syndrome, Bell’s palsy (with inhaled vaccine – which is now withdrawn)

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SUMMARY: EPIDEMICS

 Lower the:
o Infectivity (R0)
o Susceptibility (S)
 Vaccines
 Quarantine
 Fomites / other agents of transmission
 Treatment

LC: THERMOREGULATION

NORMAL BODY TEMPERATURE

 Body temperature represents the balance between heat production & heat loss
 Normal body temperature = 37°C +/- 5°C
 Optimal enzyme activity at this temperature:
o Rising body temperature accelerates enzymatic catalysis
 With each rise of 1°C, rate of chemical reactions increases about 10%
o Increased temperature denatures proteins & depresses neurons
 Children <5  convulsions at 41°C
o 43°C is the limit for life
 Tissues can tolerate low body temperatures
o This can be used in a clinical setting e.g. heart transplants – cooling isolated organs down to stop any damage

 All body tissues produce heat, but those most active metabolically produce the greatest amounts
o Most heat is generated by liver, heart, brain, kidneys & endocrine

CORE & SHELL TEMPERATURES

 Different body regions have different resting temperatures

 Shell (skin): lowest temperature
o Fluctuates
o Can range between 20°C – 40°C
o Adapts to changes in body activity & external temperature
 Core (organs within skull, thoracic & abdominal cavities: highest temperature
o Core temperature regulated; fairly constant
 Whenever shell is warmer than the external environment, body loses heat – warm blood is allowed to flush into skin capillaries

26
 o When heat must be conserved, blood largely bypasses the skin (reduces heat loss)
 Measurement of body core temperature
 Mouth & rectum: rectal temperature best clinical indicator
 Blood: major agent of heat exchange between core & shell

BALANCE OF HEAT PRODUCTION & HEAT LOSS

Heat production Heat loss

 Basal metabolism  Radiation

 Hormones  Conduction
 Muscular activity  Convection
 Temperature effect  Evaporation

 Every cell in the body is metabolising – heat is produced as a by-product

o That heat has to be lost in some way
 Body temperature remains constant as long as heat production & heat loss are balanced

FOUR MECHANISMS OF HEAT TRANSFER

 Radiation: heat transfer by infrared rays

o E.g. how a cold room warms up after it fills with people; body gaining heat as sunbaking
 Conduction: transfer of heat by direct contact
o From a warmer object to a cooler one when the two are in direct contact
 Convection: transfer of heat to surrounding air
o Warm air expands & rise; cool air falls – this substantially enhances heat transfer from body surface to the air
 Evaporation: heat loss due to evaporation of water from body surfaces
o Heat absorbed by water during evaporation = heat of vaporisation

SPA BATH

 Conduction onto the tiles

 Conduction into the water – assuming the water is cooler than the body
o If the water is warmer than the body, the body takes up heat from the water
 Shoulders will then lose than enhanced heat
 Convection of air across the shoulders

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HEAT LOSS

 Insensible heat loss:

o Basal heat loss via skin, lungs & oral mucosa
o Unnoticeable water loss occurring via continuous evaporation of water from lungs & oral mucosa & through skin
 Dissipates about 10% of basal heat production of the body
o Constant – not subject of body temperature controls
 Sensible heat loss:
o Removal of heat when temperature rises above basal levels
o Can be large – up to 30 times of insensible heat loss in vigorous muscular activity
 Emotional stress – up to 1°C rise in temperature
 Exercise – up to 2-3°C rise in temperature
o Evaporative heat loss becomes an active / sensible process the body temperature rises
 Sweating produces increased amounts of water for vaporisation
o Controlled loss via skin:
 Radiation
 Conduction / convection
 Evaporation (sweating)
 1g evaporated water removes 0.58kcal of heat

SKIN

 Skin & sympathetic nervous system – main organ for thermoregulation

 Regulated heat loss by:

ANS

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SYMPATHETIC NERVOUS SYSTEM

 Pre-ganglionic fibres synapse in sympathetic chain ganglia

 Some post-ganglionic fibres run back into the spinal nerve and innervate the skin
 Targets for SNS in thermoregulation:
o Skin:
 Blood flow
 Sweat secretion
 Arrector pili muscles
o Adrenal medulla:
 Adrenaline increases heat production

REGULATION OF BLOOD FLOW TO THE DERMIS

 Sympathetic nerve fibres  NA  a1-adrenoceptors  vasoconstriction

o Blood flow: NA  alpha-receptors
o Piloerection: Ach  M-receptors
o Sweat glands: Ach  most of body
o Sweat glands: NA  underarms / feet / palms of hands
o (Sympathetic innervation to adrenal medulla) Preganglionic fibres  Ach  N-receptors  secrete adrenaline

29
 Vasodilate / constrict by reducing / increasing activity in the sympathetic nerves
 Vasodilation increases heat transfer to the skin  increase heat loss
o In normal body temperatures, the vessels are basically half-constricted

 Increasing environmental temperature reduces heat loss via radiation or

conduction/convection
o Above 33°C, little heat loss via radiation, conduction or convection
 Evaporation is then essential to stop temperature from rising
 Sweat glands:
o Coiled glands, secreting water & ions
o Na+/Cl- reabsorbed in the duct  normally little nutrient loss
 Large secretion (hot environment)
o Fast flow reduces absorption; nutrients lost in sweat  dehydration
& ionic imbalance
 Sympathetic stimulated secretion
o Palms, feet, underarms – NA
o Elsewhere – Ach (neurotransmitter)
 Exercise:
o Perspiration: 1-2L/hour (600-1200kcal/hr)  dehydration & cramps

BODY TEMPERATURE CONTROL MECHANISMS

30
 Control centre in anterior pre-optic region of hypothalamus
o Thermoregulatory centres = heat-loss centre & heat-promoting centre
 Temperature sensors (thermoreceptors) in hypothalamus
o Receives afferent input from peripheral & central thermoreceptors in skin & abdomen
 These anticipate temperature changes (e.g. getting goose bumps after just a short time in a cold room)
 [A] control via sympathetic nervous system
o Degree of vasoconstriction in the skin
 Heat-promoting: activation of sympathetic vasoconstrictor fibres; redirects blood to deep body areas
 Heat-loss: dilation of cutaneous blood vessels + enhanced sweating
o Sweating
o Piloerection
 [B] control via somatic nervous system
o Skeletal muscle tone – skeletal muscle produces large amounts of heat
o Shivering – muscle tone reaches sufficient levels to alternately stimulate stretch receptors in antagonistic muscles
 [C] control via endocrine system (actions increase non-shivering heat production) (in kids)
o Thyroid hormones (increases BMR)
o Adrenaline (increases heat production in brown adipose tissue)
 Chemical thermiogenesis – brown adipose tissue dissipates energy by producing heat by this mechanism of
noradrenaline and adrenaline – elevates BMR and heat production

MECHANISMS OF BODY TEMPERATURE REGULATION

 Heating & cooling mechanisms not switched on or shut off

o Gradual changes in skin, blood flow, sweating etc. produces less dramatic changes in temperature

LIMITS OF SURVIVAL

 Environmental temperature of zero to 45°C

 Autonomic control of temperature – above/below this, we survive with behavioural changes (clothes, seek shade, etc.)

CORE TEMPERATURE

 Above 44°C – proteins denature / death

 Below 32°C – loss of consciousness
 Below 28°C – cardiac arrhythmias
 Below 23°C – ventricular fibrillation / death

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FEVER

 Controlled hyperthermia
o Pyrogens act on the hypothalamus, causing release of prostaglandins that reset the hypothalamic thermostat to a
higher-than-normal temperature
o As a result of the vasoconstriction, heat loss from the body surface declines – skin cools, shivering begins

 High temperature during exercise is NOT fever

 Fever: control systems not trying to correct the high temperature – but is causing it
 When there is an infection, macrophages / leukocytes produce pyrogens (interleukins, prostaglandins)
o Resets the thermostat to a higher set point
 Hypothalamus activates mechanisms to increase temperature
 Feeling cold, shivering, cold skin – heat-promoting mechanisms (e.g. shivering generating heat)
o Temperature rises & stabilises at a new set point – temperature maintained here until
natural body defences or medications reverse the disease process (cryogens prevent
fever from being excessive)
 Recovery:
o Fever “breaks” (infection reduced, pyrogens removed)
 Hypothalamus resets back to normal temp
 Body now above set point, cooling / heat-loss mechanisms activated
o Feeling hot, sweating, flushed (enhanced heat loss)
 Temperature returns to normal

 Is fever good for us?

o Fever speeds healing by increasing BMR and also appears to inhibit bacterial growth
 Mechanism of protection:
o Liver & spleen sequester iron & zinc, and less is available for bacteria (thus, inhibiting bacterial growth)
o Higher temperature reduces bacterial growth; enhances body’s repair & protective mechanisms

THERMOCONTROL IN NEWBORN

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 Newborns possess thermo-regulation:
o Vasomotor reactions
o Sweat secretion
o Non-shivering thermogenesis
 Babies have thin shell and high surface-volume ratio
o Brown adipose tissue is stimulated by catecholamines & thyroid hormones, where Na+/K+ is activated

EXTREME TEMPERATURES

 Humans adapt to extremes of temperature with behavioural changes

 Cold environment:
o Add clothes (insulation)
o Curl into ball; changing posture (reduce surface area)
o Exercise; increasing physical activity
o Move to shelter
o Hot drinks/food
 Hot environment:
o Wear light clothing (reflects heat, which is cooler than being naked)
o Spreading out
o Finding shade
o Find air movement (breeze, fan)
o Cold drinks / foods
o Use less energy (“laying low”)

COLD ENVIRONMENT

 Sympathetic nervous system – constricts cutaneous blood vessels

o For brief periods only
o Prolonged  hypoxic damage  frostbite
 Hypothermia (prolonged cold exposure)
o Respiration, HR, BP decrease
 Drowsiness
 Becomes comfortable (weirdly enough)
o Shivering stops at core temperatures of 30-32°C (body has exhausted heat-generating
capabilities)
 Progress to coma & death (cardiac arrest), when body temp approaches 21°C

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FROSTBITE

 Over the days after incident, fingers blister & puff

 Recovery very painful even with opiates
 Finally, blisters will be punctured, but may still lose a bit of tissue

HOT ENVIRONMENT

 Overexposure to hot & humid environment  lead to normal heat-loss mechanisms being ineffective
o Hyperthermia depresses hypothalamus
 At 41°C, heat loss mechanisms are suspended
o Creating vicious positive feedback cycle – increased temperature increases BMR, which increases heat production
 Can seriously damage the body

 Skin hot & dry  temperature increase

o Eventually leads to multiple organ damage – including the brain (heat stroke)
o Can be fatal unless exhaustive measures are initiated immediately – immersing body in cool water & administering
fluids

HEAT EXHAUSTION

 Extreme sweating & collapse after physical activity

o Due to dehydration (and therefore, BP)
o This is unlike heat stroke – in heat exhaustion, heat-loss mechanisms are still functional (still, can progresss to heat
stroke)
 Symptoms:
o Mental confusion
o Fainting
 High body temperature & dehydration but control systems still operating

SUMMARY

 Core temperature controlled by hypothalamus – which senses & predicts changes

 Control of heat production:
o Increased muscle tone & shivering
o Increased BMR (thyroid hormones)
o Increased metabolic rate via adrenaline
 Control of heat loss:
o Skin blood flow
o Sweating
o Piloerection
 Fever is caused by an altered thermostat set point – not an inability of control mechanisms to cope with rise in temperature

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35