Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2612_Библиотеки_им_академика_М_И_Перельмана
.pdf
Echinococcosis (hydatid disease)
PAIR
https://t.me/med1917
Zoonotic disease caused by tapeworms of the genus Echinococcus. Clinically important disease forms in humans are:
• Cystic echinococcosis (hydatid disease, hydatosis): E. granulosus. Found world-
wide. Usual host is dog. Also goats, swine, horses, cattle, camels, yaks.
• Alveolar echinococcosis: E. multilocularis. Found in northern hemisphere. Usual
hosts are foxes and rodents.
Human ingest parasite eggs via food/ water contaminated by animal faeces, or by
handing animals which are infected with the tapeworm. Disease is due to the development of cyst- like larvae in viscera, usually liver/ lungs.
cysts may be asymptomatic for many years. Symptoms and signs depend on location:
• Liver: abdo min al p ain, nau sea, hep atom ega ly, ob str uct ive j aun dice , ch olan git is, PUO.
• Lung: dyspnoea, chest pain, cough, haemoptysis.
• cns: space- occupying signs.
• Bone: an interesting osteolytic cause of knee pain, cord compression.
• Silent disease in breast, kidney, adrenals, bladder, heart, psoas.
Diagnosis USS/ CT/ MRI: avascular fluid- filled cysts ± calcification ( benign
TB, mycoses, abscess, neoplasm). Serology. Positive echinococcal an-
cyst,
Treatment Get help (including surgical). Depends on cyst type, location,
tigen.
size, and complications. Prolonged treatment (months/ years) with albendazole.
: Puncture, Aspirate, Inject (hypertonic saline/ chemicals), Re- aspirate. Beware
spillage of cyst contents: praziquantel can be given peri- operatively.
Fasciola hepatica (common liver fluke) Parasitic infection. ~2 million infected
worldwide. Highest rates of infection in Bolivia and Peru. Infective larvae develop
in aquatic snail hosts. Humans infected via contaminated water, waterplants, eg
watercress, or by eating the undercooked liver of another host animal, eg sheep,
goat. Disease caused by migration of parasite to bile ducts.
phase with migration from intestine through liver (
nausea, fever, urticarial rash, eosinophilia. Chronic phase with egg production in the
bile ducts: cholecystitis, cholangitis, pancreatitis, cirrhosis.
acute and chronic phase. Ova in stool/ bile aspirate only in chronic phase.
Triclabendazole as a single dose. Treat all suspected cases in endemic areas.
Other liver flukes: opisthorchiasis and clonorchiasis Opisthorchis and
clonorchis are liver flukes acquired by eating contaminated fish, mainly in south-
east Asia. Adult worms lodge in the small bile ducts and gallbladder.
Abdominal pain, GI disturbance, cholecystitis, cholangitis, cholangiocarcinoma.
Diagnosis Ova in stool. Treatment Praziquantel.
Tropical liver disease
An overview of the dierential diagnosis of tropical/ imported liver disease is
table
9.28
shown in
Table 9.
28
Presentation Dierential diagnosis
Jaundice/ hepatitis
Hepatomegaly Amoebic/ pyogenic liver abscess, echinococcosis, liver
Massive hepatomegaly Visceral leishmaniasis, tropical lymphoma, late- stage
Fibrosis/ cirrhosis Chronic hepatitis, schistosomiasis, alcohol, non- alcoholic
.
Tropical liver disease by presentation
Consider liver toxicity: ackee fruit (Jamaica), aflatoxins (peanuts, corn, tropical
countries without monitoring/ regulation), death cap mushroom, iron, bush tea,
methanol, copper, paraquat, pyrrolizidine alkaloids (herbal remedies).
Presentation Slow growing
Presentation Acute
2– 4
months): abdominal pain,
Diagnosis Serology in
Treatment
Presentation
22
Viral hepatitis, brucellosis, dengue, enteric fever, HIV,
leptospirosis, malaria, rickettsial infection, sepsis,
haemorrhagic fever, yellow fever
fluke, carcinoma
schistosomiasis
fatty liver disease
TB, viral
431
9 Infectious diseases
9 Infectious diseases
Neurological disease
https://t.me/med1917
432
Botulism
Neuroparalytic infection caused by neurotoxin from anaerobic, spore- forming
Clostridium botulinum (rarely C. butyricum, C. barattii). Food- borne due to toxin
production in poorly processed food (botulus is Latin for sausage), or wound botulism due to spore germination in wound (includes
of acetylcholine at neuromuscular junction causing flaccid paralysis.
Incubation up to 8d (usually 12– 36h). Febrile, descending, flaccid paralysis: diplopia,
ptosis, dysarthria, dysphagia, progressive paralysis of limbs, respiratory failure.
Autonomic signs: dry mouth, fixed/ dilated pupils, urinary/ cardiac/
No sensory signs. Diagnosis Clinical: do not delay treatment. Take samples
tion.
(serum, faeces, wound swab) for later confirmation by culture/
GI Bacteria Reference Unit (
Botulinum antitoxin (from Public Health England:
and metronidazole if wound botulism.
Tetanus
Caused by anaerobic Clostridium tetani
spores universally present in soil. Enters
body via a breach in skin. Produces a
neurotoxin (tetanospasmin) which disseminates via blood/ lymphatics and
interferes with neurotransmitter release
causing unopposed muscle contraction
and spasm (tetanus = ‘to stretch’). ~
cases/ yr in England (
neonatal tetanus important cause of preventable mortality in low– middle- income
countries.
may be trivial/ unnoticed. Incubation ~
Presentation Site of entry
Trismus (lockjaw, Greek ‘trismos’ = grinding). Risus sardonicus = a grin- like posture of hypertonic facial muscles. Opisthotonus (
by movement, injections, noise, then spontaneous. Dysphagia. Autonomic dysfunction: arrhythmias ± fluctuating
of tetanus toxin/ isolation of C. tetani.
predicts outcome. Take blood for tetanus-toxin and anti-tetanus antibodies first.
Te ta n u s i m mu n o gl o b ul i n (
Wound debridement, metronidazole. Management of spasm: diazepam/ lorazepam/
midazolam (may need high doses
administration needed for penetration of blood– brain barrier only with
latory support), dantrolene, botulinum toxin
Prophylaxis following injury:
known/ incomplete:
booster if >
TIG plus dose of vaccine in a dierent site. Precautionary travel
10
yrs since last dose.
Poliomyelitis
A highly infectious picornavirus, transmitted via faeco– oral route or contaminated food/ water. Replicates in intestine. Invades nervous system with destruction
of anterior horn cells/ brain stemirreversible paralysis. Incidence by
formation of Global Polio Eradication Initiative in
endemic in Afghanistan and Pakistan (
like prodrome in ~
stiness, tremor, limb pain. ~
respiratory failure.
40
yrs later): new progressive muscle weakness, myalgia, fatigue. Diagnosis Viral
to
culture of stool (most sensitive,
CSF. PCR can dierentiate wild- type from vaccine. Paired serology. Treatment None.
25
No sensory signs. Post- polio syndrome in ~40% of survivors (up
Vaccination Salk (inactivated, IM) or Sabin (live, oral). In previously endemic areas
200
million volunteers have vaccinated 3 billion children, meaning that 20 million
people can walk today who would have otherwise been paralysed.
IV drug use). Toxin blocks release
Presentation
GI dysfunc-
020 8327 7887
). Treatment Get help. Admit to ICU.
020 8200 4400
4
Fig 9.
47
2019
). Maternal and
3– 21
BP. Respiratory arrest. Diagnosis Clinical. Detection
Spasm causing opisthotonus
(arching of body with neck hyperextension).
tetanus, rabies, cerebral malaria, neurosyphilis, acute cerebral injury, catatonia.
© Centers for Disease Control and Prevention.
d. Prodrome: fever, malaise, headache.
fig
9.47
PCR. In UK contact
). Benzylpenicillin
). Muscular spasms induced
Treatment ICU: timely supportive care
TIG) IM (or equine antitetanus serum if not available).
IV), IV magnesium sulfate, baclofen (intrathecal
TIG if heavy contamination. If vaccination history un-
A.23 Vaccination Routine in UK (p
1988. 30
2022
).13 Presentation Incubation 7– 10d. Flu-
cases in
2022
ICU venti-
403
99
% since
. Remains
%. Pre- paralytic stage: fever, HR, headache, vomiting, neck
1
in
200
progress to paralytic stage: LMN/ bulbar signs ±
2
samples >24h apart), pharyngeal swabs, blood,
).
Rabies
https://t.me/med1917
Rhabdovirus transmitted through saliva or
fected mammal, eg bat (in
is fatal once symptoms appear. Worldwide distribution. ~
Africa/ Asia.
Presentation Incubation ~9– 90d. Prodrome: headache, malaise, odd
behaviour, agitation, fever, paraesthesia at bite/ wound site. Progresses to one of
two disease forms:
• ‘Furious rabies’: hyperactivity and terror (hydrophobia, aerophobia).
• ‘Paralytic rabies’: flaccid paralysis in the bitten limbcomadeath.
Diagnosis Clinical: potential exposure + signs of myelitis/ encephalitis (non-
progressive disease and disease >
brain, nerve tissue) or
Tre at me nt If bitten, or lick to broken skin, wash (>15min) with soap and seek urgent
CSF antibodies may oer later (postmortem) confirmation.
help. Post- exposure prophylaxis: vaccination ± rabies immunoglobulin. Experimental
treatments: ribavirin, interferon alfa, ketamine. Preventable and elimination feasible
with pre- exposure vaccination of all at risk. Vaccination of dogs can human cases.
Japanese encephalitis virus
Flavivirus spread by Culex mosquito species. Endemic transmission (~
risk) and common cause of viral encephalitis in Asia and west Pacific. Severe disease is rare (
mortality up to
1
in
250
) but leads to neurological or psychiatric sequelae in up to 50%,
30
%. Presentation Incubation 5– 15d. Most asymptomatic, or mild
fever and headache only. Severe disease: high fever, headache, meningism, altered
mental status, coma, seizures, spastic paralysis, death.
demic area. Serum/
CSF serology, PCR. Treatment Supportive. Vaccination.
West Nile virus
Mosquito- borne flavivirus with transmission in Europe, Middle East, Africa, Asia,
Australia, and Americas.
West Nile fever in ~
1
%: encephalitis, meningitis, flaccid paralysis, mortality ~10%. Diagnosis Serum/
~
CSF IGM, viral PCR. Treatment Supportive. Human vaccine awaited (
20
%: fever, headache, N&V, lymphadenopathy. Neuroinvasive in
Neurocysticercosis
Most common helminthic disease of the
epilepsy (~
Tae n ia so li u m. Consumption of infected pork leads to intestinal infection (taeniasis)
50
% of epilepsy in endemic areas, fig
and the shedding of T. s ol i um eggs in stool. Invasive disease occurs when the shed
eggs are ingested via faecal– oral transmission. Neurocysticercosis is due to larval
cysts infecting the
(cysticerci) within the brain/ spinal
cord. Epilepsy in
20
%: motor/ sensory loss, language
in ~
CNS. Presentation Determined by site and number of lesions
70
%. Focal neurology
disturbance, involuntary movements.
Also headache, visual loss, meningitis,
hydrocephalus, cognitive impairment.
Diagnosis CT/ MRI imagi ng plu s sero logy.
Tre at me nt
Seizure control (evidence
on drug choice, length of treatment,
or prophylaxis). Neurosurgical advice
if hydrocephalus/
non- calcified lesions (better penetra-
CNS than praziquantel). Beware
tion of
inflammatory response provoked by
ICP. Albendazole for
treatment— consider dexamethasone.
Tick- borne encephalitis
Flavivirus spread by tick species endemic to Northern Eurasia. Growing inci-
10 000
dence: ~
Flu- like prodrome, progressing to meningism/ encephalitis in ~
Long term sequelae in
cases/ yr. First UK case in
10
Vaccination for at risk groups. Tick bite prevention.
UK), dog (
CNS tissue, usually from the bite of an in-
95
% of human transmissions), cat, fox. Disease
3
wks are negative indicators). Viral PCR (saliva,
50 000
deaths/ yr, most in
3
billion at
Diagnosis Clinical in en-
Presentation Incubation 2–
CNS and most frequent cause of preventable
Fig 9.
demicity (orange) of Taenia solium
Reproduced with permission from WHO, Endemicity
of Taenia solium,
2016
2019
d. Asymptomatic in ~80%.
2023
).
9.48
). Caused by pork tapeworm
48
Endemicity (red) and suspected en-
2015
. http:// www.who.int/ medi acen tre/ fac tshe ets/ Endemi city _
. ©World Health Organization
Tae nia_ Soli um_ 2 015
2015
.
– 1000x 706.jpg?ua= 1
. Presentation Incubation 7– 28 days.
30
%, mortality ~1%.
%. Diagnosis Serum/ CSF serology. Treatment Supportive.
433
9 Infectious diseases
9 Infectious diseases
Eye disease
SAFE
(a)
(b)
(c)
https://t.me/med1917
434
Conjunctivitis
Common in tropical areas. Vision is normal. Dierentiation is outlined in
Table 9.
29
Common infectious causes of conjunctivitis
Cause Secretions Features Treatment
Bacterial Purulent Red and swollen
Viral Watery ± Corneal lesion Symptomatic
Trachoma
(chlamydial)
Trachoma
Leading infectious cause of blindness worldwide: visual impairment/ blindness
1.9
million,
in
Central and South America, Asia, Middle East). Caused by Chlamydia trachomatis.
Human- to- human transmission with contact, or via flies which land on nose/ eyes.
Presentation Active infection causes purulent discharge and follicular inflamma-
tion of the eyelid (
and irritate the cornea (trichiasis) (
health strategy
administration in endemic areas through International Trachoma Initiative),
cleanliness,
Mucopurulent Follicles and papillae
136
million at risk. Prevalence in endemic areas 60– 90% (Africa,
fig
9.49
: Surgery to treat trichiasis, Antibiotics (azithromycin: mass
on lid
Reproduced from Brent et al., Oxford Handbook of Tropical Medicine,
a)scarring (fig
with permission from Oxford University Press.
9.49
b)eyelids turn inwards (entropion)
fig
9.49
c)visual loss. Treatment WHO public
Environmental improvement with access to water and sanitation.13
Topical antibiotics for
Azithromycin
ical tetracycline
Immunosuppression and the eye
table
9.29
PO or top-
Facial
.
5
d
2014
,
Fig 9.
49
(a) Follicular trachoma. (b) Scarring. (c) Trichiasis.
Reproduced from Warrell et al., Oxford Textbook of Medicine,
Herpes zoster ophthalmicus
Due to reactivation of latent varicella zoster virus (p
the ophthalmic branch of the trigeminal nerve. Risk of reactivation and ocular complications in immunosuppression:
HIV, post- transplantation. Presentation: vesiculomacular
skin rash and dysaesthesia in ophthalmic division of the
trigeminal nerve (
side of nose indicates involvement of nasociliary branch of
V
1
and chance of eye involvement. Complications: corneal
fig
opacification, uveitis, ocular nerve palsy, eyelid deformity,
optic neuritis, post- herpetic neuralgia. Can be sight- threatening recognition and urgent treatment are required.
Diagnosis: clinical. Antibody staining/
ings. Treatment: oral famciclovir/ valaciclovir or systemic
aciclovir reduce complications if given within
toms. Analgesia. If retinitis
ganciclovir or foscarnet.
CMV
reti nitis
Reactivation of CMV infection (p
floaters due to inflammatory cells in vitreous, flashing
lights, scotomata, eye pain, visual loss. Peripheral lesions
may be asymptomatic. Routine examination for those
CD
4
<
100
at risk (
Fun dosc opy: gra nula r w hite dot s, h aem orrh age (
cells/ microlitre). Diagnosis: clinical.
9.5 0
). Hutchinson’s sign = lesion at tip/
PCR of skin scrap-
72
IV cidofovir ± intravitreal
401
h of symp-
). Presentation:
fig
from Oxford University Press.
400
) in
Fig 9.
ophthalmicus.
© MN Oxman, University of
Fig 9.
51
zarella pizza fundus).
9.5 1
).
2010
, with permission
50
Herpes zoster
California.
CMV retinitis (moz-
© Prof Trobe.
Can progress to an arcuate/ triangular zone of infection,
https://t.me/med1917
or can be linear following vessels/ nerve fibres. Trea tm e nt :
intravitreous ganciclovir ± oral valganciclovir. Also
foscarnet, cidofovir.
ART if underlying HIV (p
Ocular toxoplasmosis
Causes posterior uveitis. Presentation: blurred vision/
floaters. Diagnosis: clinical. Fundoscopy (
focus of choroiditis, chorioretinal scar from previous
infection, overlying vitreal haze due to inflammatory response. Multiple/ bilateral/ extensive lesions
if immunosuppression. Serology. Ocular fluid
Treatment: atovaquone (toxicity), sulfadiazine, and
pyrimethamine.
Filarial infection
Onchocerciasis (‘river blindness’)
Caused by filarial worm Onchocerca volvulus and endosymbiotic Wolbachia bac-
teria. Transmitted by the bite of infected black flies which breed in fast- flowing
rivers and streams. Second most common infectious cause of blindness worldwide: predominantly sub- Saharan Africa, Brazil, Venezuela, Yemen.
a nodule forms at the site of the bite where larvae mature to adult worms. The
female adult can release up to
• Skin disease: pruritis, altered pigmentation, lichenification, loss of elasticity.
• Eye disease: keratitis, uveitis, cataract, fixed pupil,
fundal degeneration, optic neuritis/ atrophy, visual
impairment/ loss (
• Impaired lymphatic function: lymphadenopathy,
fig
9.53
elephantiasis.
Diagnosis: visualization of microfilaria in eye or on
skin snip biopsy: a fine shaving of clean skin is incu-
0.9
bated in
for microscopic identification. Serology.
ivermectin
(depending on re- exposure risk).
% saline to allow microfilariae to emerge
150
mcg/ kg, one dose every 3– 12 months
loa due to risk of fatal encephalitic reaction.
doxycycline for Wolbachia. No vaccine available.
Loiasis (African eye- worm)
Caused by parasitic worm Loa loa. Transmitted via bite of deerflies which breed
in rainforests of west and central Africa.
sions due to angioedema (‘Calabar swellings’), myalgia, arthralgia. The adult
worm can migrate through subcutaneous (
9.5 5
) tissue: ‘Something’s wiggling in my eye, doctor’. This eerie eye trip causes
intense conjunctivitis, which heals if left alone. (Don’t treat until transmigration in the eye is over: on detecting your therapy the worm tends to panic.) Also
causes glomerulonephritis, and encephalitis.
smear, serology,
Eosinophilia.
Diethylcarbamazine (
PCR.
Tre at me nt
DEC)
kills both microfilariae
and adult worms. Risk
of encephalopathy is
related to microfilarial
load: albendazole can be
used to microfilarial
load prior to
sponse may be slow).
DEC (re-
Bite avoidance.
See also lymphatic filariasis p
398
).
fig
1000
microfilariae/ day causing:
).
Treatment:
CI if coexisting Loa
6
wks of
Presentation Recurrent pruritic le-
fig
Diagnosis Microfilariae on blood
Fig 9.
54
Migrating Loa loa in
the skin.
Reproduced from Warrell et al.,
Oxford Textbook of Medicine,
2010
, with permission from
Oxford University Press.
417
.
9.52
):
Fig 9.
52
Retinal toxoplas -
mosis.
PCR.
Presentation:
Fig 9.
53
Bilateral sclerosing
keratitis in onchocerciasis
causing blindness.
Reproduced from Warrell et al.,
Oxford Textbook of Medicine,
2010
, with permission from
Oxford University Press.
9.5 4
) and subconjunctival (fig
Fig 9.
55
Loa loa crossing the
conjunctiva
Reproduced from Warrell et al.,
Oxford Textbook of Medicine,
2010
, with permission from
Oxford University Press.
435
© Prof Trobe.
9 Infectious diseases
9 Infectious diseases
Skin disease
https://t.me/med1917
436
Dermatoses occur in 8– 23% of travellers and are the 3rd most common health
problem in travellers after diarrhoea and fever. The dierential of skin problems in
travellers is outlined in
fig
9.56
.
Skin problem
Cosmopolitan
infection (~
75
• Scabies
• Bacterial infection
• Superficial fungal
• Swimmer’s itch (p
• Herpes simplex
• Herpes zoster
Fig 9.
56
Skin problems in travellers.
Adapted from Travel Medicine and Infectious Disease, 7(3), O’Brien, BM, ‘A practical approach to
common skin problems in returning travellers’,
%)
Scabies
Caused by microscopic mite Sarcoptes scabiei.
Fou nd worl dwi de, ~
mites burrow into the epidermis and deposit eggs.
Symptoms due to an allergic reaction to the parasite.
Tra ns mi ss io n vi a d ire c t a nd p ro lo ng ed s k in - to- skin
contact. Epidemics linked to poverty, overcrowding,
and poor water supply.
turnal) pruritus, papular/ scaly rash, burrows may be
fig
9.5 7
visible (
compromised. Itch can lead to secondary bacterial
infection.
eggs/ faeces.
malathion
). Severe crusted scabies if immuno-
Diagnosis Clinical. Skin scraping for mite/
Tre at me nt To p i c a l p e r m e t h r i n 5% or
0.5
%. Ivermectin in crusted scabies.
Cutaneous leishmaniasis
Most common form of leishmaniasis. Estimated
0.6– 1
million new cases/ yr: Americas,
Mediterranean basin, north Africa, Middle East,
central Asia.
at the bite site, beginning as an itchy papule;
Presentation Lesions develop
crusts fall o to leave a painless ulcer with
a well- defined, raised border and a crusted
base = ‘Chiclero’s ulcer’ (
Skin biopsy + PCR. Tr ea tm en t Most heal in
2– 15
months with scarring (disfiguring if ex-
~
tensive). ‘New World’ disease (South America)
needs treating due to risk of mucocutaneous
disease: pentavalent antimony, eg meglumine
antimoniate, sodium stibogluconate. (See
Infectious
(more common)
Tropical disease
(~
25
Cutaneous larva migrans
•
429
, fig 9.44)
(
p
• Cutaneous leishmaniasis
430
)
• Myiasis
• Tungiasis
• Rickettsial infection
418
)
p
(
• Dengue (p
• Filariasis (p
• Leprosy
• Yaws
300
million cases/ yr. Female
416
125– 46
Presentation Severe (noc-
fig
9.5 8
). Diagnosis
p
Non-infectious
(less common)
%)
)
417
419
)
. Copyright
.)
• Arthropod bite
• Allergic reaction
• Sunburn
• Injury
• Animal bite
2009
, with permission from Elsevier.
Fig 9.
57
Scabies burrow.
Reproduced from Burge et al., Oxford
Handbook of Medical Dermatology,
2016
, with permission from Oxford
Fig 9.
58
Cutaneous leishmaniasis with
central crusting.
Reproduced from Lewis- Jones, Paediatric
Dermatology,
2010
University Press.
, with permission from
Oxford University Press.
Myiasis
https://t.me/med1917
Infection with fly larvae/ maggot. Can aect living
and necrotic tissue. In South and Central America
the human botfly lays its eggs on mosquitoes which
deposit them when they bite. In sub- Saharan
Africa the tumbu fly lays its eggs on clothing
which then transfer to skin.
swelling. May have sensation of movement within
the lesion. May open to reveal larval breathing
fig
9.59
tubes (
of larvae in lesion.
). Diagnosis Clinical. Identification
Treatment Petroleum or pork
fat asphyxiate the maggot causing it to protrude
further out of the skin enabling removal with tweezers. Care: backward- facing spines in botfly larvae
may prevent complete removal unless done surgically. Ensure tetanus vaccination
is up to date.
Tungiasis
Infection of the skin by the sand/ jigger flea Tunga penetrans. Acquired (usually
walking barefoot) in sandy soil, rainforests, and banana plantations in South and
Central America, sub- Saharan Africa, Asia, Caribbean.
papule on the feet. May be visible extrusion of eggs. Black crusting when flea dies.
Diagnosis Clinical. Treatment Topical dimeticone, self- limiting.
Leprosy (Hansen’s disease)
Caused by slow- growing, acid- fast Mycobacterium leprae which aects skin,
nerves, and mucous membranes. Incubation
nose/ mouth during close and frequent contact. Classified as:
• Multibacillary (‘lepromatous’): immune response, bacilli, + ve smear.
• Paucibacillary (‘tuberculoid’): immune response, granulomata with bacilli,
smears may be –ve.
Hypersensitivity reactive episodes occur: type
2
(er ythema nodos um lepr osum and organ / joint inflammation, eg neuritis, lymph-
type
adenitis, arthralgias). Free multibacillary treatment via
WHO since
1985, 174 087
skin lesions (
1995
: prevalence by 99% (
in
2022
).13 Presentation Hypopigmented
fig
9.60
, less well demarcated than vitiligo), sensory loss, thickened nerves, nodules, plaques,
nasal congestion, epistaxis, muscle weakness, paralysis, neuropathic ulcers. Eye involvement: chronic
iritis, scleritis, episcleritis, corneal sensation (
nerve palsy), blinking and lagophthalmos (
palsy), trauma from eyelashes (trichiasis).
Clinical, + ve skin smear, skin biopsy. Serology unreli-
Tre at me nt WHO multidrug therapy: rifampicin
able.
600
mg/ month, dapsone
month and
6
50
months for paucibacillary. Treat type 1 and 2 reactions
100
mg daily. Duration: 1yr for multibacillary,
with steroids.
Yaw s Chronic granulomatous disease caused by
Treponema pertenue. Found in humid/ rainforest areas
in Africa, Asia, Latin American, Pacific. Associated
with socio- economic conditions. Transmission via
direct contact.
illoma. If untreated will ulcerate (
Presentation Primary disease = pap-
disease: yellow skin lesions, dactylitis.
complications do not occur.
tinguishable from syphilis (Treponema pallidum). Dualpath platform (
current and past infection.
azithromycin
DPP) assay can distinguish between
PO.
Presentation Painful
5– 20
yrs. Transmitted via droplets from
1
(erythema of skin lesions, neuritis),
5.2
million in
V
VII nerve
Diagnosis
mg OD, clofazimine
Diagnosis Serology is indis-
PCR. Treatment Single- dose
fig
9.61
300
mg/
). Secondary
CVS
and CNS
Fig 9.
59
Myiasis.
Reproduced under Creative Commons
CC
0 1.0
Universal Public Domain from
https:// comm ons.wikime dia.org/ wiki/ File:Miasi
s_ hu man.jpg
Presentation Painful, itchy
Fig 9.
60
Leprosy: hypopig-
mented macules.
Courtesy of Prof Jayakar Thoma.
Fig 9.
61
Ulcero- papillomatous
yaws.
CDC/ Dr. Peter Perine.
437
9 Infectious diseases
9 Infectious diseases
Pyrexia of unknown origin (
https://t.me/med1917
438
This cha pter gi ves g uidan ce o n hund reds of py rexia- causing infections; but what
should you do if your patient has a fever that you cannot explain? Pyrexia of unknown
PUO)24 has a dierential of >
origin (
ally be given an infective diagnosis (depending on your corner of the globe). ~
remain undiagnosed, but in most of these the fever will resolve within
Diagnostic criteria
Pyrexia >3wks with no cause identified after evaluation in hospital for 3d or ≥3
out- patient visits.
Fever may also be undiagnosed in specific subgroups despite appropriate evalu-
3
d, including negative cultures at ≥2 days:
ation for
• Nosocomial
• Immunodeficient
•
HIV PUO
PUO
Patient hospitalized for >48h with no infection at admission.
PUO
Pyrexia in HIV infect ion la sting 3d as an inpatient or >4wks as an outpatient.
History
PUO are due to common diseases with atypical presentation. Consider all de-
Most
tails as potentially relevant. Include: travel (
medication, recreational drug use, obstetric/ sexual history, family history (
Examination
Confirm fever. Pattern of fever is rarely helpful (contrary to the textbooks, most malaria has no specific pattern). Full head-to-toe examination. Do not forget: mouth, genitals, skin, thyroid, lymphatic system, eyes/retina, temporal arteries (
Investigation
Extent of investigation depends on immune status and how well the patient is.
• Blood tests FBC, U&E, LFT, CRP, ESR, electrophoresis, LDH, CK, ANA, ANCA, rheumatoid
HIV test, malaria smear, interferon- gamma release assay for TB (p
factor,
• Microscopy and culture Blood ≈3, urine, sputum (including AFB), stool, CSF.
• Imaging CXR, abdominal/ pelvic USS, venous Doppler. Consider: CT(PA), MRI, echo
TOE). Fluorodeoxyglucose- PET (FDG- PET) highlights areas of glucose uptake in-
(
cluding tumour and inflammation. It may aid/ direct diagnosis in up to
• Other Hepatitis serology, CMV, EBV, autoimmune screen, cryoglobulins, toxoplas-
mosis, brucellosis, Coxiella, lymph node biopsy, endoscopy, temporal artery biopsy.
Table 9.
30
PUO dierential according to history and examination findings
History Dierential
Animal contact
Cough
Nasal symptoms Sinusitis,
Confusion
Arthralgia
Weight loss Malignancy, vasculitis, TB, HIV, IBD, thyrotoxicosis
Family history Familial Mediterranean fever
Drug history
Examination Dierential
Conjunctivitis Leptospirosis, relapsing fever, spotted fever, trichinosis
Uveitis
Mouth Dental abscess, Behçet’s disease,
Lymphadenopathy
Rash
Hepatomegaly
Splenomegaly Leukaemia, lymphoma,
Renal Chronic pyelonephritis, perinephric abscess, renal tumour
Epididymo- orchitis
Brucellosis, toxoplasmosis, Bartonella, leptospirosis,
TB, PE, Q fever, enteric fever, sarcoidosis, legionnaire’s disease
TB, Cryptococcus, sarcoid, carcinomatosis, brucellosis, enteric fever
SLE, infective endocarditis, Lyme disease, brucellosis, TB, IBD
Drug- induced fever (~
TB, sarcoid, adult Still’s disease, SLE, Behçet’s disease
Lym phom a,
HIV, EBV, SLE, vasculitis, Still’s disease, endocarditis
TB, EBV, malignancy, malaria, enteric fever, granulomatous hepa-
titis,
EBV, rheumatoid arthritis, sarcoid, enteric fever, relapsing fever
TB, lymphoma, EBV, brucellosis, leptospirosis
PUO
)
200
diseases. 15– 30% of these patients will eventu-
Pyrexia in patient with <
GPA, relapsing fever, psittacosis
TB, EBV, CMV, HIV, toxoplasmosis, brucellosis, Bartonella
Q fever, visceral leishmaniasis
500
neutrophils/ microlitre.
p
410
), diet, animal contact, changes in
7– 10
d after new drug)
CMV, IBD
TB, brucellosis, infective endocarditis, CMV,
20
% will
4
wks.
table
table
9.3 0
).
390
).
50
% of PUO.
Q fever, p sittacos is
9.3 0
).
Eliciting the weird and the wonderful
https://t.me/med1917
Listen to your patient You have two cultures to master: the host and the
pathogen. Prolonged immersion in both may be needed.
Ask Do not expect to find apposite questions such as these in any other textbook:
1
‘Have you delivered any septic babies in the last year?’ Impress and cure your
obstetrician friends who tell you that ‘I’m so depressed about not being able
to shake o this flu’, and who have forgotten about transfer of brucellosis from
baby to obstetrician.
2
‘Are your carp well at present?’ Mycobacterium marinum skin infection.
3
‘Where exactly did you get that sheep- skin rug?’ Anthrax from handling in-
fected animal hides.
4
‘Who has been licking your face recently?’ Pasteurella multocida.
5
‘Did you have a stray pig living under your house when the monsoon started?’
+
standing water + mosquitoes = Japanese encephalitis.
Pigs
6
‘Has your pet hedgehog lost weight?’ Salmonella.
7
‘Did you develop your headache after you adopted your pet magpie?’ Zoonotic
transmission of Cryptococcus neoformans causing meningitis.
8
‘Has your pet seal given you a nasty nip?’ Sealpox virus.
9
‘Was it windy when you visited the Grand Canyon?’ Valley fever from
Coccidioides spores in Western
10
‘Did your goat miscarry last year?’ Coxiella burnetii.
11
‘Were you drunk when you fell in that rose bush?’ Sporotrichosis ‘Rose
gardener’s disease’; disseminated disease with alcohol misuse disorder.
12
‘Can I see your pet lobster: he may be the cause of your bad hand?’ Lobsterman’s
hand, an erysipeloid infection from Erysipelothrix. Pet lobsters have a grand
pedigree. Gérard de Nerval used to take his pet lobster for walks, on a blue silk lead, beside the Seine (
9.62
). A lobster, he said, is, ‘serious- minded and quiet,
US soil.
fig
doesn’t scratch or bark like a dog, and knows all of
the secrets of the deep’. His lobster’s mission was to
combat the Philistinism chaining us all to mediocrity.
Ask also, ‘Where have you been?’ Though you will
not be absolved of thought, even when the answer is,
‘Southend’. It may be a question of amnesic stopovers.
Or perhaps your patient is an airport baggage- handler,
Fig 9.
62
‘Is your pet lobster
well?’ (Gérard de Nerval).
bitten by a hitch- hiking mosquito. And even when there has been no travel to
the tropics, global warming and globalization are ensuring that the tropics are
travelling to us. To the first writers of medical books, Paradise was just beyond
the Far East, and the world was a disc surrounded by oceans of blue water. But
the world moves on, tarnished, tawdry, and trashed; and Paradise is evolving with
ever more serpents in the garden, beguiling us with an abundance of answers to
our great questions.
Don’t give up If the culture is negative, tests may need repeating. Perhaps the
organism is ‘fastidious’ in its nutritional requirement or requires a longer incubation? Even if culture is achieved, it may be that the organism grown is flora not
pathogen. If culture fails, look for antibodies or antigen.
for identification, but it is far from infallible; beware of inhibitors, contamination,
PCR is increasingly used
and a primer that is not as unique as your patient.
Remember Sherlock: ‘My mind,’ he said, ‘rebels at stagnation. Give me problems,
give me work, give me the most abstruse cryptogram or the most intricate analysis, and I am in my own proper atmosphere. I can dispense then with artificial
stimulants. But I abhor the dull routine of existence. I crave for mental exaltation.
That is why I have chosen my own particular profession,— or rather created it,
for I am the only one in the world.’
The Sign of the Four, Arthur Conan Doyle,
No, Sherlock, you are not; you have infectious disease physicians for company.
1890
439
9 Infectious diseases
.
10
https://t.me/med1917
Neurology
Contents
Neurology at the bedside
Where is the lesion?
Drugs and the nervous system
Cerebral blood supply
Testing peripheral nerves
Dermatomes and peripheral nerves
Some common presentations
Headache
452
Migraine
454
Blackouts
456
Transient global amnesia
Vertigo and dizziness
Tinnitus
458
Hearing loss
Functional neurological disorders
Acute bilateral leg weakness
Abnormal involuntary movements
(dyskinesia)
Diseases and conditions
Stroke:
Subdural haematoma
Extradural (epidural) haematoma
Cerebral venous thrombosis (
Idiop athic in tracrani al hyper tension
Delirium (acute confusional state)
Dementia
Alzheimer’s disease (AD)
Epilepsy: diagnosis
Epilepsy: management
Parkinsonism
Multiple sclerosis (MS)
Space- occupying lesions (
Mononeuropathies
Bell’s palsy
Polyneuropathies
Guillain– Barré syndrome
Autonomic neuropathy
Motor neuron disease (
Bulbar palsy
Cervical spondylosis
Myopathy
Myasthenia gravis (MG)
Lambert– Eaton myasthenic
syndrome (
Neurofibromatosis
Syringomyelia
Chiari malformations
Retroviruses and neurology
We thank Thomas Hughes and Marc Edwards, our Specialist Readers for this chapter.
459
464
Acute assessment and
management
Intracerebral haemorrhage (
Tra ns ie nt is ch a em ic at ta ck (
Prevention
Rehabilitation
Subarachnoid haemorrhage
(
SAH
466
470
472
)
474
482
486
490
496
498
500
503
506
LEMS
)
508
510
512
442
458
504
512
446
476
488
492
501
MND
484
508
448
456
SOL
500
444
450
460
462
ICH
)
468
TIA
)
469
Fig 10.
1
Sir Roger Bannister
the first ever subat the age of
476
CVT
)
494
)
502
student at Oxford University, and graduated
)
478
the following year. He went on to become a
478
prominent academic neurologist, conducting
480
research into the autonomic nervous system,
which he regarded as his greatest achievement.
Autonomic activity and running are, of course, intimately linked, as Bannister reflected in a more
poetic manner than the usual ‘fight or flight’
cliché: ‘As a child I ran barefoot along damp,
fresh sand by the seashore. The air there had a
special quality. . . The sound of breakers shut out
all others, and I was startled, almost frightened,
by the tremendous excitement a few steps could
create. It was an intense moment of discovery of
a source of power and beauty that one previously
hardly dreamt existed.’ In
publicly of his sense of irony at being diagnosed
with Parkinson’s disease.
25
. At that time he was a medical
Photo by Keystone/ Getty Images.
CBE (1929– 2018)
4
- minute mile on 6 May
2014
, Bannister spoke
ran
1954
513
Соседние файлы в папке Библиотека им академика М.И. Перельмана