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
Leptospirosis (Weil’s disease)
Definitive host (Cat)
through placenta
d
https://t.me/med1917
Pathogen ic leptospi re spirochaetes belonging to the sub group Leptospira interro gans.
250
pathogenic serovars. Chronic renal infection of carrier animals: rodent, cattle,
>
pigs. Spread by water/ soil/ food contaminated by infected animal urine.
Incubation ~
like symptoms. Mild/ subclinical in ~
leptospiruric) phase: conjunctival suusion, myalgia (
itis,
1886
all severe disease.)
gov.uk/ guida nce/ lep tosp ira- refere nce- unit- servi ces
Serology.
7
d (2– 30d). 1st (acute/ septicaemic) phase: fever, non- specific flu-
AKI, pulmonary haemorrhage, ARDS, myo/ pericarditis. (Weil’s disease described in
90
%. Followed by recovery or 2nd (immune/
CK), jaundice, meningitis, uve-
: fever, jaundice splenomegaly, renal failure, CNS symptoms. Term now applied to
Diagnosis In UK18 via National Leptospirosis Service (https:// www.
). Culture (blood/ CSF) + ve during 1st phase.
PCR. Tre atm en t Mild: doxycycline, azithromycin. Severe: ceftriaxone, IV
Presentation
penicillin. Conflicting evidence of benefit for steroids in severe disease.
Yersinia pestis (plague)
Gram –ve, obligate intracellular pathogen transmitted by small animals and their
fleas by bite, direct contact, inhalation, or ingestion (rare). ~
Presentation Incubation: 3– 7d. Flu- like symptoms, then one of three disease forms:
1
Bubonic: most common form. Yersinia pestis enters at bite and travels via
lymphatics. Inflamed, painful lymph node is termed ‘bubo’ and can suppurate.
2
Septicaemic: direct spread without ‘bubo’, or advanced stage after ‘bubo’.
3
Pneumonic: lung disease. Most virulent, least common. Usually from advanced bu-
bonic form but can then transmit via droplets to other humans without fleas/ animals.
Diagnosis Culture bubo fluid, blood, sputum. Rapid antigen testing available.
300
cases/ yr worldwide.
Treatment Reduces mortality from 60% to <15%: streptomycin, tetracycline.13
Toxoplasmosis
fig
Caused by protozoan Toxoplasma gondii. Found worldwide. Life cycle (
Infection is lifelong (~⅓ of population).
Presentation Asymptomatic in ~90%. Self- limiting cervical lymphadenopathy,
HIV may cause reactivation (p
396
9.36
).
low- grade fever if normal immune system. Disseminated disease if immunosuppressed: cerebral abscess, encephalitis, choroidoretinitis, myocarditis, myositis, pneumonitis, hepatitis. Congenital infection: pregnancy loss, neurocognitive deficit, retinal
Diagnosis In UK via Toxoplasma Reference Laboratory (
damage.
IgG = previous exposure (high avidity IgG suggests infection >
Serology:
ago, used in pregnancy);
IgM; IgA in cord serum = congenital infection. PCR: blood/ CSF/ urine/ amniotic
sistent
fluid/ aqueous/ vitreous humour.
IgM = acute infection, false + ve or chronic infection with per-
Tre at me nt If eye disease, immunosuppressed, or neo-
0179 228 5058
3– 5
months
nate: pyrimethamine + sulfadiazine + folinic acid. Corticosteroids for eye inflammation. Spiramycin reduces vertical transmission. Prophylaxis: co- trimoxazole.
Echinococcosis (hydatid disease) p
431
. Rabies p
433
. Hanta virus p
422
.
421
9 Infectious diseases
).
).
Cysts in tissues of
Fig 9.
36
Oocysts in cat faeces can stay in the soil for months, where rats eat them. The rats get infected,
and, under the direction of Tox o p la s m a in the amygdala, the rats lose their fear of cats, and so get eaten
in turn. So the parasite ensure success by facilitating a jump from intermediate to definitive host. How
does the parasite overwhelm the innate fear of cats? By causing a sexual attraction to normally aversive
cat odour through limbic activity.
intermediate host
Ingested cysts in
infective meat (raw
or undercooked)
Infected
fetus
Tachyzoites
transmitted
Cysts ingested
by cat
From Fernan do M onro y: www
Intermediate
hosts
Unsporulated
oocytes passed
Oocytes in food, water
or soil ingested by
intermediate
host
Contaminated
food/water
2
in faces
Sporulate
oocysts
.nau.edu/ ~fpm/ res ea rch/ res.html
9 Infectious diseases
Viral haemorrhagic fever (
VHF
Lassa, Ebola and Marburg:
Countries with confirmed human case
https://t.me/med1917
422
Viral haemorrhagic fever (VHF) is a term used for severe, multi- organ disease in
which the endothelium is damaged, and homeostasis is impaired. Haemorrhage
complicates the disease course and can be life- threatening.
viral subtype is shown in
Table 9.
22
VHF classification (HF = haemorrhagic fever)
Virus family Disease (virus subtype) Details
Filovirus Ebola
Marburg
Arenavirus
Lassa fever (Lassa)
Argentinian HF (Junin)
Bolivian HF (Chapare,
Machupo)
Brazilian HF (Sabia)
Venezuelan HF (Guanarito)
Bunyavirus Crimean- Congo HF
Hanta
Rift valley fever
Flavivirus Dengue
Yellow fever
The Advisory Committee on
Dangerous Pathogens (
classifies a pathogen as Group
(highest) when it causes severe
human disease, with high risk
of spread, and no eective
prophylaxis or treatment.
19 Marburg, Lassa, and
Ebola,
Crimean- Congo haemorrhagic
CCHF) are all Hazard
fever (
4
haemorrhagic fever vir-
Group
uses, as was smallpox. They are
largely confined to Africa (
9.3 7
), with the exception of CCHF
which occurs in the Middle East,
Africa, Eastern Europe, and Asia.
Risk assessment for
Assess for possible transmission and fever.
• Tra ns mi ss i on :
1
Trav el to en de m ic ar ea <21 day s (r ural for Lass a fe ver; cav es/ primates/ antelopes/
bats for Ebola/ Marburg; tick/ animal slaughter for
2
Trav el to k no wn ou t bre a k (http:// www.pro medm ail.org).
3 Contact with infected specimen.
• Fev er: >37.5°C in the past 24h.
If possible transmission and fever consider ‘high possibility’ (≠high probability),
PPE (see BOX ‘Equipment’). Inform local infectious disease team and con-
isolate,
tact the Imported Fever Service (
bleeding, and uncontrolled
)
table
9.22
.
See Ebola,
p
See Marburg,
p
See Lassa,
South American
infection in travellers. Incubation
Resemble Lassa fever. Severe disease with
bleeding in ~
vaccine available for Junin virus
CCHF, p
See
423
Rodent host. Incuba tion
with renal syndrome: fever, headache,
AKI.
toms, and
drome: bilateral interstitial pulmonary infiltrates,
30– 40
mortality
Endemic in Africa.
self- limiting febrile illness. <
VHF classification by
423
p
423
423
VHFS are rare causes of
2– 16
⅓. Supportive treatment. Live
2
d– 8wk. Causes: 1 HF
2
Hanta virus pu lmonary sy n-
%. Supportive treatment
80
% asymptomatic or
2
% CNS involve-
ment/ haemorrhagic
See
p
416
See
p
416
ACDP)
4
Ebola and/or Marburg
Endemic Lassa
Endemic Lassa, and Ebola outbreak
Lassa virus present, sporadic human cases
Fig 9.
37
Lassa, Ebola, and Marburg risk in Africa.
Reproduced with permission from Viral haemorrhagic
fevers: origins, reservoirs, transmission and guidelines, Crown
copyright
2018
UK
VHF
fig
in the
0844 778 8990
D&V also need isolation and advice if relevant contact.
s
. Contains public sector information licensed
under the Open Government Licence v
CCHF).
) for VHF investigation. Bruising,
d.
GI symp-
3.0
.
Ebola
https://t.me/med1917
2– 21
Incubation
with mortality. Largest epidemic (
Zaire ebolavirus):
d (usually 3– 12d). Evidence for fruit bats as reservoir. Outbreaks
28 646
cases and 11
Cytokine activationendothelial damage, oedema,
coagulopathy, tissue necrosis, multi- organ failure.
Tra ns mi ss io n f ro m i nd ex cas e via m uc ou s m em branes, or contact with body fluids (including burial
contact), viral shedding in semen.
• Undifferentiated (0– 3d). Fever (>38°C axillary), my-
algia, weakness, anorexia, headache, sore throat.
May not look unwell.
• GI (4– 10d). Epigastric/ abdominal pain, liver ten-
N&V, hiccups, diarrhoea, hypovolaemia.
derness,
• Late organ stage (>10d). Haemorrhagic: petechiae,
ecchymoses, mucosal haemorrhage,
treme weakness, confusion, agitation, bradypsychia, coma. Other: hypoglycaemia,
electrolyte abnormalities, secondary infection, shock,
• Post- infection: arthralgia, hepatitis, orchitis, transverse myelitis, meningitis, uve-
itis, vision/ hearing impairment, social isolation, psychological eects.
Diagnosis PPE (see BOX ‘Equipment’) if high possibility (see
WCC, plts, AST > ALT. IgM (~day
blood/ urine/ saliva/ throat swab.
citation, correct electrolytes/ coagulation/ glucose, treat secondary infection, nutrition.
Tra ce c on ta ct s, su pp or t fa mi ly. E xp er im en ta l a nd e vo lv in g th er ap ie s: a nt i-
immunotherapy with blood/ plasma from survivors, monoclonal antibodies (
114
), Ebola vaccine (rVSV- ZEBOV, Ebola ça sut! trial). Ethics Randomization
mAb
versus compassionate use: is it ethical to withhold even potentially beneficial therapy
to a control group with a life- threatening condition? Is observational data gained
through the compassionate use of experimental therapy sucient to guide clinical decisions? Where should resources be directed to improve outcome: drug development
or basic healthcare provision, eg would the capacity to check K
Marburg, Lassa, and
CCHF
Dierentiating features are given in
Table 9.
23
Dierentiation between VHF
VHF Clinical features
Marburg
Lassa
CCHF Tick- borne. Sudden- onset prodrome. Haemorrhagic stage common, develops
Incubation typically
Ebola/ Marburg suggested by liver tenderness
80
~
ferent epidemics
Observational data shows response to ribavirin if given in first
rapid ly, but us ually sh ort- lived
Sacrifice
This book choses to celebrate Dr Ameyo Stella Adadevoh, a Nigerian physician whose diagnostic acumen protected a nation. On a post- take ward round
in Lagos in
never having seen the disease before. She isolated and treated the patient des-
2014
, she recognized the index case of Ebola virus in Nigeria despite
pite neither her hospital nor her country being ready to do so, and in the face of
litigation threats. In order to save others, and for ‘the greater public good’ she
sacrificed herself, dying from Ebola on
from a death toll far greater than
whom we also pay our deepest respects). And so we go forward in the hope that
when our own mortality salience is activated and we are not in the warm, comfortable bed of the octogenarian we all desire to become, our existential anxiety
can be buered by the memory of Dr Adadevoh who confers greater meaning to
our doctoring lives: we did what we could to help the most.
2014– 2016
) due to Ebola virus (EVD, formally
323
deaths in Guinea, Liberia, and Sierra Leone.
Equipment
• Double gloves
• Fluid- repellent gown
Presentation
GI bleeding, haemoptysis. Neurological: ex-
3
), IgG (~day 7), reverse transcriptase PCR on
• Ful l- length plastic apron
• Head cover (surgical cap)
• Fluid- repellent footwear
• Ful l fac e sh iel d
• Ful l- repellent respirator
• Meticulous removal.
DIC, multi- organ failure, death.
BOX
‘Risk assessment’).
Exclude mal aria. Tr ea tm en t Supportive: fluid resus-
RNA agents,
+
improve mortality?
table
9.23
.
5– 9
d. Clinically identical disease course to Ebola.
20
25– 80
%. Exudative pharyngitis. Convalescent hearing loss.
2– 3
d. Ribavirin used in treatment (evidence).
19
August
8
(including 4 other healthcare workers to
%. Variable mortality in dif-
6
2014
. Thus she protected Nigeria
d
REGN- EB
423
9 Infectious diseases
3
,
9 Infectious diseases
Gastroenteritis: an overview
https://t.me/med1917
424
Gastroenteritis = diarrhoea (± vomiting) due to enteric infection with viruses, bacteria, or parasites. Diarrhoea can be defined as:
• Acute diarrhoea: ≥3 episodes partially formed or watery stool/ day for <
• Dysentery: infectious gastroenteritis with bloody diarrhoea.
• Persistent diarrhoea: acutely starting diarrhoea lasting >
• Traveller’s diarrhoea: starting during, or shortly after, foreign travel.
• Food poisoning: disease (infection or toxin) caused by consumption of food/ water.
Food poisoning is notifiable in the UK (www.gov.uk/ hea lth- pro tect ion- team).
Gastroenteritis can be classified according to infectious aetiology (
predominant clinical presentation (
Table 9.
24
Gastroenteritis by infectious aetiology
Infection Organism Incubation Notes Page
Virus
~
Bacteria
~
Parasites
<
50– 60
30– 40
2
%
%
%
Norovirus
Rotavirus
Astrovirus
Adenovirus
Sapovirus
CMV ~
Salmonella
(non- typhoidal)
Campylobacter2– 5d
E. coli
Shigella
Staphylococcus
aureus
Clostridium
perfringens
Clostridium
difficile
Listeria
Vibrio cholerae2h– 5d
Yersinia
enterocolitica
Bacillus cereus30min– 15h
Giardia
Cryptosporidium1– 12d
Entamoeba
histolytica
Cyclospora
cayetanensis
Trichinella
Trichuriasis
Intestinal flukes
d.
table
9.25
, also see p
1
d
1– 3
d Aects nearly all children by age 5yrs.
4– 5
d
3– 10
d
1– 3
d
3– 12
12– 72
1– 10
d
(usually
1– 2
d S. sonnei most comm on. Deadly epidemics
30
min– 6h
6– 24
3– 70
4– 7
d
1– 3
wks
2– 4
wks (can be
years)
~1wk
1– 2
d Enteral at 1– 2d. Parenteral at 2– 8wks:
3
months
~
4
d— months Eg Fasciolopsis buski
Important cause of epidemic gastroenteritis.
600 000– 1
Routine , childhood ( live) vaccine i n UK
Often less severe than norovirus
Enteric adenovirus. Mainly children
Children. Not common in food- borne disease
Usually asymptomatic. If immunosuppres-
wks
sion: colitis, hepatitis, retinitis, pneumonia
Under- cooked eggs, poultry, meat
h
Under- cooked meat, cross- contamination,
unpasteurized milk, water
Bloody diarrhoea if Shiga- toxin producing E. coli (
3– 4
d)
Under- cooked beef, unpasteurized milk
most common.
with S. dysenteriae in low- income countries
Unpasteurized milk/ cheese, uncooked food.
Multiplication leads to toxin production
Raw meat. Inadequately reheated food
h
Antibiotic- associated diarrhoea. Sporeforming therefore pe rsists: wash your hands
Cold meat, soft cheese, refrigerated pâté.
d
Diarrhoea, fever, myalgia. Severity in
immunosuppression and pregnancy (bacteraemia, fetal loss)
Human and aquatic reservoirs. Epidemics due
to inadequate environme ntal management
Main source is undercooked pork. Most
infection in young children
Leftover food, rice. Emetic or diarrhoeal
toxins.
Intestinal parasite. Cyst transfer via
infected faeces, eg contaminated water.
Malabsorption
Transfer via infected faeces. Symptoms and
severity with immunosuppression, eg HIV
Asymptomatic carrier, intestinal disease
and/ or extra- intestinal disease (liver, skin,
lung, brain)
Transfer via infected faeces. May have
relapsing course
larval migration, facial swelling, myocarditis, encephalitis
Whipworm. Dysentery with heavy infection
255
).
million cases/ yr in UK
STEC
) eg
0157
. Can cause
table
HUS
d.
9.24
) or
426
426
397
,
401
427
427
387
,
.
425
,
427
427
384
426
407
385
426
427
428
397
,
428
428
429
429
429
Table 9.
https://t.me/med1917
25
Gastroenteritis by clinical presentation
Diarrhoea without blood (enteritis) Diarrhoea with blood (dysentery)
Norovirus Shigellosis (bacillary dysentery)*
Rotavirus
Astrovirus
Enteric adenovirus
Enterotoxigenic E. coli Clostridium difficile
Enteropathogenic E. coli Yersinia enterocolitis
Toxin- producing Staph. aureus Entamoeba histolytica (amoebic dysentery)
Cholera Trichuriasis (whipworm)
Clostridium perfringens
Giardia
Cryptosporidium
Cyclospora cayetanensis
*Milder disease may present as diarrhoea without blood.
Traveller’s diarrhoea
Diarrhoea aects 20– 60% of travellers.20,21 High- risk areas: South Asia, Central
and South America, Africa. Major cause = enterotoxigenic E. coli.
Prevention Boil water, cook thoroughly, peel fruit and vegetables. Avoid ice,
salads, shellfish. Drink with a straw. Hand washing with soap may risk.
Presentation Most diarrhoea is during first week of travel. Symptoms are often
unreliable indicators of aetiology but the following may be indicative:
• Enterotoxigenic E. coli: watery diarrhoea preceded by cramps and nausea.
• Giardia lamblia: upper GI sy mptoms , eg bl oatin g, bel ching .
• Campylobacter jejuni and Shigella: colitic symptoms, urgency, cramps.
Duration of diarrhoea: most <
Tre at me nt
• Oral rehydration. Clear fluid and oral rehydration salts. Home- made oral rehy-
dration recipe:
• Antimotility agents, eg loperamide, bismuth subsalicylates. Avoid if severe pain
or bloody diarrhoea as may indicate invasive colitis.
• Antibiotics: usually not indicated. Balance risk (resistance, side eects, car-
riage non-typhoid salmonella,
6
teaspoons of sugar + half teaspoon salt in 1L clean water.
if rapid cessation of diarrhoea needed and/ or limited access to sanitation/
healthcare. Reduce diarrhoea from ~
lergy, medication, and destination: azithromycin
fluroquinolone resistance, particularly
or rifaximin
• Consider admission if severe dehydration/ signs of shock.
200
mg TDS for 3d.
Prophylaxis Not recommended as severe disease and long- term sequelae rare,
risk of C. difficile. Consider in immunosuppressed (transplant,
GI pathology (IBD, ileostomy, short- bowel), risk with dehydration (sickle cell,
CKD). Care with interactions with usual medications.
• Ciprofloxacin
• Norfloxacin
• Rifaximin
• Bismuth subsalicylate 2 tablets QDS (62– 65% protection, 1st line in US).
500
mg OD (80–
400
mg OD (75– 95% protection).
200
mg every 12– 24h (72– 77% protection).
Persistent diarrhoea Investigate if >
tory markers, stool microscopy for ova/ cysts/ parasites (historically
may not actually improve diagnostic yield, time intensive), molecular testing for
(pre- defined) microbes. of persistent diarrhoea = Giardia (most common diagnosis, send
syndrome is a diagnosis of exclusion (in up to
Do not forget: malaria, HIV.
PCR), Entamoeba histolytica, Shigella. Post- infectious irritable bowel
Enterohaemorrhagic E. coli
Campylobacter enterocolitis*
Salmonella enterocolitis*
CMV
1
wk, 10%>1wk, 5% >2wks, 1% >30d.
HUS
in
O157:H7
E. coli.) and benefits. Considered
3
100
% protection).
to ~1.5 days. Choice depends on al-
SE Asia), ciprofloxacin
500
mg OD for 3d (risk of
d or dysentery: FBC, U&E, LFT, inflamma-
30
%).
500
mg BD for 3d,
HIV, chemotherapy),
3
samples but
425
9 Infectious diseases
9 Infectious diseases
Gastroenteritis: specific infections
https://t.me/med1917
426
Diarrhoea without blood
Norovirus Single- stranded RNA virus. Highly infectious. Transmission by contact
with infected people, environment, food (~
tious
lasting
GI disease, ~
600 000
24– 72
h: acute- onset vomiting, watery diarrhoea, cramps, nausea. Virus shed
in stool even if asymptomatic. Numerous genotypes and unknown longevity of
immunity repeat infection occurs. Diagnosis: clinical, stool sample reverse tran-
PCR. Treatment: supportive, anti- motility agents, usually self- limiting.
scriptase
Rotavirus Double- stranded RNA virus. Wheel- like appearance on EM ‘rota’.
Commonest cause of gastroenteritis in children (~
Presentation: incubation ~
dominal pain. Diagnosis: clinical, antigen in stool. Treatment: supportive. Routine
vaccination in
munosuppressed and changing nappies. Live vaccine delay vaccination if in utero
UK (p
403
biological agents with active transfer across placenta (eg infliximab, adalimumab).
Enterotoxigenic E. coli Gram –ve facultative anaerobe. Disease due to heat- stable
or heat- labile toxin which stimulates Na
of all infective diarrhoea, ~
3
d. Watery diarrhoea, cramps. Lasts ~3– 4d. Diagnosis: clinical, identification of toxin
from stool culture. Tre atm en t: supportive. See
Clostridium perfringens (type A) Gram + ve, anaerobe. Produces enterotoxin.
Spores survive cooking and germinate during unrefrigerated storage.
breaks/ yr in
UK. Presentation: sudden- onset diarrhoea, cramps, usually lasts <
Diagnosis: stool toxin, quantification of faecal bacteria. Treatment: supportive. -
toxin of C. perfringens type
ease, pain, bloody diarrhoea, septic shock. - toxin is sensitive to trypsin proteolysis
so risk with trypsin inhibition by sweet potatoes, ascaris infection occurs in
New Guinea (‘pigbel’), central/ south America, south- east Asia, China.
Cholera Vibrio cholerae is a Gram –ve, aerobic, ‘comma- shaped’ flagellated motile
vibrating/ swarming rod. Found in faecally contaminated water. Serovars
cause disease. ~
Presentation: incubation
190 000
h) diarrhoea (‘rice- water’ stool), vomiting, dehydration, metabolic acidosis, circulatory
collapse, death. Diagnosis: clinical: death due to dehydration from watery diarrhoea
5
yrs, or any watery diarrhoea age >5yrs during known epidemic. Identification
age >
of serovars
ation recommended. Tre at me nt :
treat
NG if vomiting. IV fluids if severely dehydrated: Ringer’s lactate or
ORS (beware K
01
or
0139
13 up to
80
%. Needs safe water. Adults may need 1L/ h initially: oer
+
) up to
diarrhoea: doxycycline (single dose
susceptibility (azithromycin in children/ pregnancy). Zinc shortens illness in children
10– 20
mg/ 24h). Prevention: cholera loves filth: clean water (and clean politics) abol-
(
ishes it. Oral cholera vaccines (
production capacity. Antibiotic prophylaxis breeds resistance.
10
%). Most common cause of infec-
cases in England/ yr. Presentation: 12– 48h after exposure,
50
2
d. Watery diarrhoea and vomiting for 3– 8d, fever, ab-
%). Most infected by 5yrs.
). Virus shed in stool post vaccine careful hygiene if im-
+
80
, Cl-, and water eux into gut lumen. ~20%
% of traveller’s diarrhoea. Presentation: incubation 1–
BOX
‘Traveller’s diarrhoea’ (p
425
2– 30
).
out-
24
C can cause a necrotizing enteritis with fulminant dis-
O
1
cases in
2014
(fig
9.3 8
2
h– 5d. ~75% asymptomatic but shed bacteria. Profuse (1L/
). Last indigenous case in UK in
and O
1893
in stool. Rapid dipstick testing available but culture confirm-
oral rehydration salts (WHO/ UNICEF ORS sachet) will
100
mL/ 5min.
0.9
200
mL/ kg in first 24h. Antibiotics in severe dehydration to
300
mg) or tetracycline (3d course) guided by local
56– 94
% ecacy in adults) dependent on logistics, cost,
% saline plus
Fig 9.
38
Cholera: areas
reporting outbreaks
2010– 2014
.
Reproduced with
permission from World
Health Organization,
Countries reporting
cholera,
2010– 2015
©World Health
Organization
2016
Countries reporting cholera,
Countries reporting cholera,
2015
2010–14
www.who.int/ gho/ epidem ic_ d
isea ses/ chol era/ epidem ics/ en/
. http://
139
h.
.
.
On the mode of communication of cholera
STEC
https://t.me/med1917
Fig 9.
39
Death’s Dispensary,
1866
George Pinwell,
Image in the Public Domain.
1
Knowledge of the microscopic cause of disease is not required for public health
measures to succeed (Vibrio cholerae was identified by Robert Kock in
2
Even the most parochial are capable of life- saving action when assisted by a
doctor in command of the facts.
3
Influential friends help. Snow remained largely unknown until the
On the Mode of Communication of Cholera was republished by Wade Hampton
Frost, first professor of epidemiology at John Hopkins School.
4
Randomization (Broad St pump versus an alternative water supply) is king.
.
Diarrhoea with blood (dysentery)
Shigella (sonnei, flexneri, dysenteriae, boydii) Gram –ve anaerobe. Presentation:
watery or bloody diarrhoea, pain, tenesmus, fever
MSM. Complications: bacteraemia, reactive arthritis (~
in
toxin- producing dysenteriae). Diagnosis: stool culture.
Tre at me nt : supportive. Nutrition: green bananas (short- chain fatty acids in colon),
zinc if age <
Guided by local susceptibilities (ciprofloxacin, azithromycin). Avoid antidiarrhoeal
6
yrs, vitamin A. Antibiotics if systemically unwell, immunosuppressed.
agents: risk of toxic dilatation.
Enterohaemorrhagic/ Shiga- toxin producing E. coli (
facultative anaerobe. Produces veratoxins which are ‘Shiga- like’ due to similarity
with Shigella dysenteriae. Presentation: incubation
HUS in up to
colitis.
for Shiga toxin.
10
% (p
Tre at me nt Supportive. Do not give antibiotics: risk of HUS.
Campylobacter Gram –ve, spiral- shaped rod. Presentation: incubation 1– 10d (usu-
2– 5
d). Bloody diarrhoea, pain, fever, headache. Complications: bacteraemia,
ally
hepatitis, pancreatitis, miscarriage, reactive arthritis, Guillain– Barré. Diagnosis:
stool culture.
in invasive cases, refer to local susceptibilities (macrolide, doxycycline, quinolone).
PCR/ enzyme immunoassay. Treatment: supportive. Antibiotics only
Salmonella enterocolitis (non- typhoidal) Gram –ve, anaerobic, motile bacilli.
Presentation: diarrhoea, cramps, fever, usually within
infection (<
10
%) can cause bacteraemia/ sepsis, meningitis, osteomyelitis, septic
arthritis. Diagnosis: stool culture.
no evidence of benefit for antibiotics in healthy people. Consider in severe/ extraintestinal disease according to local susceptibilities (quinolone, macrolide).
Yersinia enterocolitica Gram –ve rod. Presentation: incubation 4– 7d. Diarrhoea,
fever, pain (may mimic appendicitis), vomiting. May last
nodosum, reactive arthritis (~
agglutination titres. Treatment: antibiotics in severe disease depending on local
susceptibilities (aminoglycosides, co- trimoxazole, quinolone).
See also: Staph. aureus pre- formed toxin (p
Clostridium difficile (p
407
In
1854
, at 40 Broad St, London, a child became
ill with diarrhoea, dying on
2
September. Her
mother rinsed her soiled nappies into the house
drains where faulty brickwork allowed mixing
with the water supply of the Broad St pump
fig
9.39
). From this confluence sprung the discip-
(
line of Public Health. The ensuing deaths from
cholera clustered around the Broad St pump, as
detailed by the local doctor, Dr John Snow. He
used his now famous Voronoi diagram showing
the deaths within a ‘line of nearest pump’ to
motivate the parish vestry: ‘In consequence of
what I said, the handle of the pump was removed
the following day’, so inaugurating the control
of cholera. These events illustrate a number of
truths:
1883
1930
1– 2
d after exposure. Lasts ~5– 7d.
2
% of flexneri), HUS (Shiga-
PCR/ enzyme immunoassay.
), eg
O157:H7
Gram –ve
3– 8
311
). Diagnosis: stool culture. PCR/ enzyme immunoassay
PCR. Treatment: supportive. Meta- analysis shows
1
month after diarrhoea). Diagnosis: stool culture,
).
d. Diarrhoea, haemorrhagic
12– 36
h of exposure. Invasive
1– 3
wk. Also erythema
384
), GI parasites (pp
).
s when
428– 9
427
9 Infectious diseases
),
9 Infectious diseases
Gastrointestinal parasites
Amoebic colitis
(e)
https://t.me/med1917
428
Giardiasis
fig
9.40
Giardia lamblia (
spread from infected drinking water/ food/ fomites.
Asymptomatic in the majority. Incubation
flatulence, bloating, pain, malabsorption. Duration of symptoms typically ~
traveller’s diarrhoea (
and trophozoites. Intermittent shedding so multiple samples (
may sensitivity. Faecal immunoassay.
Duodenal fluid aspirate analysis.
transmission. Metronidazole (treatment failure in up to
) is a flagellate protozoan. Faecal– oral
Presentation
1– 3
wks. Diarrhoea,
2– 6
wks. Most common diagnosis if persistent
p
425
). Diagnosis Stool microscopy for cysts
PCR for diagnosis/ subtype.
Tre at me nt Hygiene to prevent
3
)
20
%),
tinidazole (single dose), albendazole ( side eects, simultaneous
treatment of other parasites), nitazoxanide. Lactose- intolerance
develops in
in endemic areas due to likelihood of re- infection.
20– 40
%. No treatment for asymptomatic disease
Cryptosporidium
fig
9.41
Apicomplexan protozoan (
). Ingestion of oocytes in
infected water. Asymptomatic or self- limiting diarrhoea
in immunocompetent hosts. Chronic/ severe diarrhoea
with immunosuppression:
hypogammaglobulinaemia, immunosuppressive therapy.
HIV (p
396
), transplantation,
Amoebiasis
fig
9.42
Protozoan Entamoeba histolytica (
100 000
/ yr. Faecal– oral spread. Boil water to destroy cysts.
~
Presentation
) ~10% world’s population, mortality
Fig 9.
immunofluorescence.
© S Upton, Kansas Univ.
• Asymptomatic passage of cysts in ~90% (‘luminal amoebiasis’).
• Intestinal amoebiasis: dysentery (often insidious onset/ relapsing), pain, colitis, ap-
pendicitis, toxic megacolon. Amoeboma = inflammatory abdominal mass, usually
RIF ± obstruction.
caecal/
• Extra- intestinal (invasive) disease. Amoebic liver abscess in ~1%. Single mass con-
taining ‘anchovy- sauce’ pus. High swinging fever,
or (cholestatic).
50
% have no history of amoebic dysentery. Also peritonitis (rup-
RUQ pain/ tenderness. LFT normal
ture of colonic abscess), pleuropulmonary abscess, cutaneous/ genital lesions.
Fig 9.
40
Giardia: the
only diplomonad to
trouble us.
41
Cryptosporidium
Excretion in
the faeces
(g)
Encystation
in colon
(f)
Asymptomatic
colonization
Fig 9.
42
The lifecycle of Entamoeba histolytica is in two stages: cysts and trophozoites. Cysts (10–
15
µm across) typically contain four nuclei (upper right image). During excystation in the gut lumen,
nuclear division is followed by cytoplasmic division, giving rise to eight trophozoites. Trophozoites
10– 50
µm across) contain one nucleus with a central karyosome (lower right image). Trophozoites
(
inhabit the caecum and colon. Re- encystation of the trophozoites occurs in the colon, and excretion
of cysts in faeces perpetuates the lifecycle.
Left hand image from Hutson C et al., ‘Molecular- based diagnosis of Entamoeba histolytica infection’,
Expert Reviews in Molecular Medicine,
University Press. Upper and lower right images courtesy of Prof S Upton, Kansas University.
Cyst
(a)
(d) Trophozoites
(invasive)
(h)
Ingestion by human
of contaminated
food and water
(b)
Excystation in
small intestine
(c)
(amoebic)
(i)
Liver abscess
1(9
): 1– 11,
1999
, reproduced with permission from Cambridge
Diagnosis Microscopy of stool (cysts and trophozoites, fig
https://t.me/med1917
sample. Enzyme immunoassay: antigen detection as adjunct to microscopy, antibody
detection in extra- intestinal disease.
logically identical but non- invasive E. dispar.
amoebic dysentery and invasive disease. Diloxanide furoate: luminal agent,
to destroy gut cysts, given in asymptomatic gut carriers and symptomatic disease, in
addition to other treatment. Abscess may require (image- guided) drainage.
Cyclospora
Coccidian protozoan Cyclospora cayetanensis. ~
cases/ yr in
rhoea, weight loss, marked fatigue, low- grade fever in ~
Self- limiting after
Autofluorescent oocytes in stool (appear blue- green under
UV fluorescence, fig
UK. Presentation Flu- like prodrome, watery diar-
7– 9
wks in immunocompetent. Diagnosis
9.43
), PCR. Treatment Co- trimoxazole.
Nematodes (soil- transmitted helminths and Trichinella)
• Roundworm: Ascaris lumbricoides ~1
billion aected, Trichinella spiralis (contaminated meat source).
• Whipworm: Trichuris trichiura,
million aected.
• Hookworm: Necator americanus, An -
cylostoma duodenale ~
fected.
• Thread worm: eg Strongyloides stercoralis,
30– 100
mil lion a ected.
One of most common infections worldwide, aects poor and deprived (
Parasites live in intestines, producing
1000
s egg/ day in faeces. Humans infected
by eggs (ascariasis, trichinosis) or larvae
(Ancylostoma) in contaminated food; or
via direct penetration of the skin (hookworm, Strongyloides).
Diarrhoea, abdominal pain, blood/ protein loss, impaired
growth/ cognitive development. Pruritus/ urticaria if migration involves skin (Strongyloides,
sion (ascariasis, hookworm, Strongyloides) can lead to
a Loeer- like syndrome: cough,
ptysis, consolidation, eosinophilia. Other tissue invasion
(trichinosis): myalgia, conjunctivitis, photophobia, meningitis, encephalitis, neuropathy.
in stool sample (
ology/
Table 9.
Drug Mechanism Indication
Mebendazole Binds free beta- tubulin, causing glucose uptake Roundworm, whipworm, hookworm
Albendazole Ascariasis, hookworm (Strongyloides)
Ivermectin Cl
Pyrantel
pamoate
Piperazine
Praziquantel
Taeniasis (tapeworm) Includes Taenia solium (pork, 2– 8m, 50
Taenia saginata (beef,
millions of eggs).
glottids) through anus/ in faeces.
Praziquantel, niclosamide.
See also toxoplasmosis (p
fig
9.45
PCR. Treatment table
26
Anthelmintic drugs
). Eosinophilia. Strongyloides ser-
-
permeability, hyperpolarization, paralysis
Depolarizing neuromuscular blockade causing
spastic paralysis of worm
Binds GABA muscl e recepto rs; flac cid paral ysis
Alters cell permeability, causing paralysis
4– 12
Presentation No or mild GI symptoms, tapeworm segments (pro-
9.42
), aspirate, or biopsy
PCR can distinguish E. histolytica from morpho-
Tre at me nt Metronidazole/ tinidazole for
50
imported
25
%.
Fig 9.
oocysts fluorescence.
600– 800
700
million af-
Fig 9.
44
Larva currens: a serpiginous
maculopapular rash pathognomonic of chronic
fig
9.44
).
strongyloidiasis. Oedema, an urticarial appearance, and speed of migration (>
guish this from cutaneous larva migrans which
is caused by animal (dog/ cat) hookworm.
Reproduc ed from John son et al., Oxford Handbook
of Expeditio n and Wilderness Medicine,
Presentation
fig
SOB, wheeze, haemo-
Diagnosis Clinical, eggs
9.26
.
m,
100 000
eggs/ worm), Taenia asiatica (Asian, 4– 8m,
permission from Oxford University Press.
9.44
). Lung inva-
Fig 9.
≈
Strongyloides, ascariasis
Single dose in threadworm, round-
worm, hookworm
(Ascariasis), pregnancy
Schistosomiasis, tapeworm
45
40
µm) & w orm (20cm).
Courtesy of Prof S Upton,
Diagnosis Eggs/ proglottids in faeces. Treatment
421
), schistosomiasis (p
430
), cysticercosis (p
10
d course
43
Cyclospora
CDC DPDx.
5
cm/ h) distin-
2016
, with
Ascaris eggs (45
Kansas University.
000
eggs/ worm),
433
).
429
9 Infectious diseases
9 Infectious diseases
Schistosomiasis and liver disease
https://t.me/med1917
430
Schistosomiasis (bilharzia)
Human (a) Snail releases infectious
Snail
schistosome cercariae into
fresh water
(h) Snails infected
(g) Eggs hatch in
fresh water
(f) Eggs released in
urine or stool
Fig 9.
46
Schistosomiasis life cycle.
Reproduced from: Coltart C, CJM Whitty. Schistosomiasis in non- endemic countries. Clin Med
9
. https:// doi.org/ 10.7861/ clinm edic ine.15- 1- 67. Copyright ©
Caused by blood- flukes (trematode worms) of the genus Schistosoma (
290
million people in 78 countries required treatment in
fig
9.46
. Disease develops after contact with contaminated freshwater (swimming,
in
washing). Symptoms are due to an immune complex response to the migrating parasite (Katayama syndrome), or chronic parasite egg deposition in body tissues.
Presentation ~50% asymptomatic or non- specific symptoms. Clinical syndromes:
• Larval penetration: pruritic papular rash (‘swimmer’s itch’).
• Migration of schistosomules: Katayama syndrome 2– 8wks after exposure: fever,
urticaria, diarrhoea, cough, wheeze, hepatosplenomegaly, eosinophilia.
• Host response to egg deposition:
• Intestinal disease: pain, diarrhoea, blood in stool, (granulomatous) hepatomegaly,
splenomegaly. Heavy chronic infection can cause bowel perforation, hyperplasia,
polyposis, liver fibrosis, portal hypertensionvarices.
• Urogenital disease: haematuria, dysuria, ureteric fibrosishydronephrosis, CKD,
bladder fibrosis/ cancer, genital lesions, vaginal bleeding, dyspareunia, vulval
nodules, haemospermia, prostatitis.
• Lung disease: pulmonary hypertension and cor pulmonale.
• CNS dis ease: rare, a cute lower limb p araple gia, t ransver se (‘t ravelle r’s’) m yeliti s.
Diagnosis Ova in urine (S. haematobium) or faeces (all other species) is specific, but
50
sensitivity <
% if light infection. Serology for egg antigen becomes + ve once mature flukes lay eggs will b e –ve in Kataya ma fever. B owel/ bladder histology. Chronic
S. haematobium: bladder calcification on
thick bladder wall on
4
h (30mg/ kg in S. japonica and S. mekongi). Steroids for Katayama fever. If
ated by
eosinophils >
persist for years).
Table 9.
3
months after treatment look for other helminths (+ ve serology can
Prevention Prophylactic praziquantel for at- risk groups.
27
Parasite species and geographical distribution
Disease form Species Geography
Intestinal
S. mansoni
S. japonica
Other
Urogenital
S. haematobium
(b) Cercariae
penetrate human skin
(c) Immature
schistosomes migrate
through body
(d) Schistosome
maturation
(e) Adult worms mate
and produce eggs
2015
Royal College of Physicians. Reproduced with
2018
. The life cycle is shown
USS. Tr eat me nt Two d os e s o f pr a zi q u an t el
AXR, renal obstruction, hydronephrosis ±
Africa, Middle East, Caribbean, Brazil,
Venezuela, Suriname
China, Indonesia, Philippines
S. mekongi: Cambodia, Laos; S. guineensis/
intercalatum: rainforests of central Africa
Africa, Middle East, France
Can cause
Katayama
fever and/or
Loeer’s
syndrome
2015;15:67
permission.
table
20
mg/ kg PO separ-
9.27
–
).
Соседние файлы в папке Библиотека им академика М.И. Перельмана