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Examination
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Rash
• Maculopapular: dengue, chikungunya, EBV, HIV seroconversion, VHF.
• Purpuric: dengue, meningococcal infection, plague, DIC, VHF.
• Ulcer/ eschar: Chagas’, Yersinia pestis, Rickettsiae
fig
9.24
), anthrax, tropical ulcer.
(
Jaundice Viral hepatitis, severe falciparum malaria,
enteric fever, leptospirosis, relapsing fever, typhus,
bartonellosis
Hepatosplenomegaly See table
HIV, enteric fever, brucellosis, leptospirosis, rickettsial
infection, relapsing fever, schistosomiasis, amoebic
liver abscess, trypanosomiasis, visceral leishmaniasis.
Investigation
Directed by travel history and examination. In undifferentiated fever:
• Malaria film/ rapid diagnostic testing (p
• HIV test (p
• FBC: lymphopenia in viral infection including HIV; eosinophilia in parasitic/ fungal eg
• Blood culture ×2: prior to antibiotics, LFT. Consider: save serum, specific serology,
395
).
soil- transmitted helminths, filariasis, schistosomiasis, hydatid disease; platelets
in malaria, dengue,
or
EDTA sample for PCR.
HIV, typhoid, severe sepsis.
Support
• Local infectious diseases team (never underestimate the wisdom of your on- call
microbiologist). Travel fever diagnostic website:
• Public Health England imported fever service:
• National Travel Health Network and Centre (NaTHNaC)/ TravelHealthPro: www.trav
elhe alth pro.org.uk
Enteric fever: typhoid and paratyphoid
~20 million cases and
200 000
imported from India, Pakistan, and Bangladesh. Caused by related, Gramnegative strains of ‘typhoidal’ Salmonella spp.:
• Ty ph oi d (~75– 90%): Salmonella typhi.
• Parat yphoid (~10– 25%, less severe): Salmonella sero type Paratyphi A > B > C.
The bacteria invade intestinal mucosa. Dissemination occurs without a primary diarrhoeal response. This distinguishes ‘typhoidal’ from
‘non- typhoidal’ serovars of Salmonella (
contaminated water/ food. Incubation
are required to cause illness. Can be asymptomatic (but shed organism).
Symptoms Fatigue, headache, anorexia. Marked fever, ‘stepwise’ (rising through each
day with progressive peaks) in <
constipation. Rose spots in ~
terial emboli to dermis). Diarrhoea (‘pea- soup’) and hepatosplenomegaly in
Complicated disease in up to
hepatitis, pneumonia,
DIC, CNS involvement (delirium, meningism, encephalitis, cere-
bellar signs, fits, coma), eye complications (corneal ulcer, uveitis, neuritis, thrombosis).
Diagnosis Isolation of S. typhi from: blood (take multiple cultures of 10– 15mL in
10
d to sensitivity), bone marrow, intestinal secretions, or stool (sensitivity
first
1
st week). Serology has sensitivity and specificity. (Widal test is –ve in
after
~
30
% of culture- proven cases.) LFT. PCR (not routine).
Treatment Azithromycin ± IV ceftriaxone. >70% imported from Asia are resistant
to fluoroquinolones. Fever takes median
of organism. Antipyretics, fluid management, nutrition.
3
mg/ kg IV then 1mg/ kg/ 6h for 8 doses (limited data).
sone
Vac cine Ty21a (oral, live, CI: imm uno supp ress ion , pre gna ncy) or Vi (IM, capsular vac-
50– 80
cine). ~
% eective for ~3yrs. Limited/ no protection against paratyphoid.
VHF,
9.28
: viral hepatitis,
413
).
deaths per year worldwide, ~
p
424
6– 30
20
%. Abdominal pain, relative bradycardia, cough,
25
% (salmon- coloured, 1– 4cm, blanching, due to bac-
10
%: intestinal haemorrhage/ perforation, myocarditis,
5– 7
d to respond due to intracellular niche
Fig 9.
24
Eschar from African
tick- bite fever.
Reproduced from Caplivski and
Scheld, Consultations in Infectious
Disease
2012
, with permission
from Oxford University Press.
www. fevertravel.ch
0844 778 8990
.
500
/ yr in UK mostly
D&V- inducing
). Transmission is faecal– oral from
d (most 10– 20d). ~10
000
organisms
2
nd week.
CNS disease: dexametha-
411
9 Infectious diseases
9 Infectious diseases
Malaria: diagnosis
Not applicable
https://t.me/med1917
412
Epidemiology
• 3.2 billion people at risk in 95 countries = half the world’s population (fig
•
228
million cases in
• Africa: 93% of malaria cases, 94% of deaths (most age <5yrs).
• Most common tropical disease imported into UK, ~
• ~20% fever in travellers from Africa presenting to UK hospitals is due to malaria.
• Plasmodium falciparum is the most prevalent parasite in Africa and responsible
for most malaria deaths worldwide (= ~
• Plasmodium vivax is the dominant parasite outside of sub- Saharan Africa.
• Preventable and treatable: incidence by 9% and deaths by 32% since
• Partial immunity widespread in endemic countries.
2018
with
405 000
deaths.
2000
cases/ yr.
75
% of malaria presenting in UK).
Malaria parasites
100
Malaria parasites belong to the genus Plasmodium. >
cause human disease (
table
9.19
). Transmission occurs through the bite of an in-
species exist of which 5
fected Anopheles mosquito. Only female mosquitoes transmit Plasmodium as only
females require a blood meal for egg development. Transmission in the absence of
a mosquito is rare: vertical (congenital transfer from mother to child), transfusion,
organ transplantation, needle- sharing.
Malaria incidence,
2018
0
<
0.1
0.1
to <
1
1
to
10
>
10
to
50
>
50
to
100
>
100
to
250
>
250
No malaria
Fig 9.
25
Countries with malaria transmission.
Reproduced with permission from World Health Organization, World malaria report
Table 9.
19
Malaria species in humans
Species
P. falciparum
fig
9.26
)
(
P. vivax
fig
9.27
)
(
P. malariae
fig
9.28
)
(
P. ovale
P. knowlesi
Reproduced from Detels et al., Oxford Textbook of Global Public Health,
Health Organization
Average incubation (range)
12
days (6 days–
6
months)
14
days
(days– years)
30
days
28
days– years)
(
11– 16
days (years)
9– 12
days
2018
. https:// www.who.int/ publi cati ons/ i/ item/ 978924 1565 653
Persistent
liver stage
No Africa, India, South East Asia, Indonesia,
Distribution
Oceania, Central America, Middle East
Yes South Asia, South and Central
America, Africa, Middle East
No Africa, South and Central America,
South East Asia
Yes Africa
No South East Asia
2015
, with permission from
Oxford University Press.
9.25
2010
2018
).
.
. © World
Fig 9.
26
P. fa l ci pa ru m sau sa ge-
like gametocytes in
RBC.
© S Upton, Kansas Univ
Fig 9.
27
P. vivax ring partly
hidden by Schuner’s dots.
Stained and examined in the field
by
JML.
Fig 9.
28
P. malariae ring and
band forms from
© S Upton, Kansas Univ.
2
specimens.
The life cycle of malaria is
Plasmodium
transmission
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dependent on both humans
and mosquitoes (
Sporozoites are transferred to
fig
a human host when an infected
mosquito bites. These travel
via the bloodstream to the
liver where maturation occurs
to form schizonts containing
30 000
merozoite ospring. If
~
a dormant stage exists (vivax,
ovale, see
adequately treated, merozoites
table
9.19
), and is in-
can be released from the liver
weeks, months, or years later
causing recurrent disease. The
rupture of schizonts releases merozoites which enter
niche!’). In the
RBC, merozoites form larger trophozoites and erythrocytic schizonts
(poor prognostic indicator if seen on blood film). The rupture of erythrocytic schizonts produces the clinical manifestations of malaria.
Clinical features
Consider in anyone with a fever who has previously visited a malarial area
fig
9.23
), regardless of prophylaxis.
(
Presentation P. f al ci pa ru m has a minimum incubation of 6 days and most com-
3
monly occurs within
months of return from an endemic area. Take a careful travel
history: country, area of travel, date of return. Do not forget to ask about stopovers.
Symptoms are non- specific: fever, headache, malaise, myalgia, diarrhoea, cough.
Fever patterns are described but only occur if rupture of infected
ized: alternate day for P. falciparum, P. vivax, P. ovale (‘tertian’); every
P. malariae (‘quartan’).
Examination Fever, hepatosplenomegaly, pallor; often unremarkable. If diagnosis
Most patients have no specific fever pattern.
is delayed or severe disease then may present with jaundice, confusion, seizures.
Diagnosis
Immediate blood testing is mandatory in the
• Microscopy of thick and thin blood smear. Sensitive and specific in experienced hands.
• Rapid diagnostic test (RDT) detection of parasite antigen. Used for initial screen if
expert microscopy is unavailable, eg out- of- hours. Used in addition to (not instead
of) blood film.
Results should be available within
negative: repeat at
serial blood films are negative. : dengue, typhoid, hepatitis, meningitis/ enceph-
HIV, viral haemorrhagic fever. Care in pregnancy: thick films can be negative
alitis,
despite parasites in the placenta. Seek expert help.
If P. falciparum (or P. knowlesi) estimated % parasitized red cells should be given:
• >2% = chan ce of se vere di sease (indi catio n for pa renter al trea tment see pp
• >10% = severe disease.
FBC (anaemia, thrombocytopenia), creatinine and urine output (AKI), clotting
Other:
DIC), glucose (hypoglycaemia), ABG/ lactate (acidosis), urinalysis (haemoglobinuria).
(
12– 24
Malaria is notifiable to public health:
Errors to avoid
• Failure to consider diagnosis. • Delay in blood film/ RDT.
• Inadequate travel history. • No serial blood film if first test negative.
• Belief prophylaxis prevents all malaria. • Inadequate treatment (pp
• Belief presents with a fever pattern. • Inappropriate treatment (pp
• Non- specific symptoms not recognized. • Fa il ur e to an ti ci pa te / treat complications.
Based on Beeching et al., Returned travellers. In: Principles and Practice of Travel Medicine,
9.29
).
Initial
human
host
In utero
4
h. If malaria is suspected but blood film is
UK:
st
1
vector
Liver
infection
Blood
infection
RBCS (‘What a fantastic
sporozoites
nd
2
vector
Fig 9.
29
Malaria lifecycle.
RBCS is synchron-
Next human
host
3
rd day for
h and after further 24h. Malaria is unlikely if three expert
414– 15
).
www.gov.uk/ hea lth- pro tect ion- team
414– 15
).
414– 15
).
2013
Wiley and Sons. Copyright ©
2013
by Blackwell Publishing Ltd.
, John
413
9 Infectious diseases
9 Infectious diseases
Malaria: treatment
https://t.me/med1917
414
Falciparum malaria
Risk of deterioration admit to hospital. Treatment
uncomplicated, or severe. Features of severe disease are:
disease is
• Impaired consciousness/ seizures (consider LP).
• AKI (oliguria <0.4mL/ kg/ h, creatinine >
• Shock (BP <90/ 60) = ‘Algid malaria’. • Acidosis (pH <7.3).
• Hypoglycaemia (<2.2mmol/ L).
• Pulmonary oedema/ ARDS.
Poor prognostic indicators: peripheral blood schizonts (
tate, age, severe jaundice, organ dysfunction.
Uncomplicated falciparum malaria
Artemisinin combination therapies (ACT) achieve rapid clearance of parasites by
combined action at dierent stages of the parasite cycle (
1
Artemether- lumefantrine: 4 tablets (4×20/
UK (+ pregnant >
line in
Redose if vomiting <
2
Dihydroartemisinin (DHA)- piperaquine: 4 tablets (4×40/
60
kg). Take >3h pre and post food to prevent excess peak levels. SE: QTc.
>
ACT not available:
Options if
• Atovaquone- proguanil: 4 tablets OD for 3 days. Parasite clearance ~66% after 3d,
GI SE in ~
25
• Oral quinine sulfate
450
chonism’: nausea, deafness, ringing in ears.
Resistance to ACT is emerging in Asia.
Failure rates with antifolate drugs mean Fansidar® is no longer used.
Chloroquine is not used in the treatment of falciparum malaria.
%. Do not use for treatment if used for prophylaxis.
mg TDS if pregnant) for 7d. Parasite monitoring required. Can cause ‘cin-
Severe P. falciparum malaria
Give urgent parenteral treatment. Artesunate is treatment of choice. Meta-
analysis shows reduction in mortality of
preventing
Artesunate regimen (adult)
2.4
of
medication. Side eects
limiting)— check Hb
ately, treatment should be started with quinine. It is safe to overlap/ combine with
artesunate when it is available.
Quinine regimen (adult)
Loading dose 20mg/ kg over 4h. Then 10mg/ kg every 8h for next 48h or until patient can swallow (dose every
tion or if
Give with
fects: cinchonism (see earlier in topic), hyperinsulinaemia.
Manage in a high dependency setting. Capillary permeability so vulnerable to pul-
monary oedema if over- filled. Lactate levels may reflect intravascular obstruction
rathe r than circ ulating hyp ovolaem ia. Mon itor: blood gl ucose every
infusion), Hb, clotting, electrolytes, creatinine. Daily parasite counts are sucient
will fluctuate with the life cycle of the parasite (
treatment may not indicate treatment failure. Given the rapid action of artesunate,
exchange transfusion is no longer considered to oer any additional benefit.
Pregnancy Little evidence on use/ safety of artesunate. On balance of risk (preg-
nancy loss, pulmonary oedema, maternal mortality), artesunate should be given.
94
deaths for every
mg/ kg IV at 0h, 12h, 24h and then daily for up to 5d. Converted to a full course
ACT (see uncomplicated falciparum earlier in topic) when able to tolerate oral
IV needed >
7
d oral doxycycline (clarithromycin in children/ pregnant ). Side ef-
11 depends upon whether the
• Hb <80g/ L.
265
µmol/ L).
13
wks), with high- fat food to absorption. SE: vomiting.
2
h post dose.
600
mg TDS for 5– 7d plus doxycycline
39
1000
adults treated.12
: delayed haemolysis
d post treatment. If artesunate is not available immedi-
12
48
h if patient has renal failure or hepatic dysfunc-
h). Convert to
600
mg PO TDS to total quinine course 5– 7d.
• Spontaneous bleeding/ DIC.
• Haemoglobinuria.
• Parasitaemia >10%.
p
413
), elevated serum lac-
p
413
120
mg) at 0, 4, 8, 24, 36, 48, and 60h. 1st
% (CI: 25– 50%) compared to quinine,
7– 21
d post- treatment (usually self-
p
413
) and an increase in first 36h of
):
320
mg) OD for 3d (weight
200
mg OD (or clindamycin
4
h (2h if quinine
NB:
Non- falciparum malaria
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P. vi va x , P. o va le , P. ma la r ia e, P. k now l es i
• If mixed infection with falciparum, treat as falciparum.
• If severe/ complicated non- falciparum disease, treat as severe falciparum.
• If uncomplicated disease, treat with ACT as uncomplicated falciparum.
Chloroquine can be used for susceptible non- falciparum disease. Dosing in adult:
620
mg base at 0h,
• Do not use if P. falciparum cannot be excluded.
• Be aware that ACT may work more quickly on both fever and parasite count.
• Chloroquine resistance exists in P. vivax (Papua New Guinea, Indonesia).
In addition to other treatment, P. vivax and P. ovale require eradication of liver
hypnozoites with primaquine:
• P. vivax: adult 30mg (0.5mg/ kg) daily for
• P. ovale: adult 15mg (0.25mg/ kg) daily for
Risk of haemolysis with primaquine in G
310
mg base at 6– 8h,
expert advice for dosing/ monitoring patients with
Malaria prevention
Vector control for all people at risk of malaria. Includes:
• Source reduction by destruction of mosquito breeding sites (ie standing water).
• Long- lasting insecticidal nets. These should be provided free of charge and with eq-
uity of access. Nets last for ~
resistance is an increasing concern, should dual agents be used?
• Indoor residual spraying, eective for 3– 6 mon ths wh en >80% of houses included.
• Sterile male mosquito release. Estimated to initially require 20 males/ human to be
protected ~
• Genetic modification to develop mosquitoes that are not susceptible to malaria
64
bil lion s terile mosqu itoes world wide.
(and other) parasites. Requires modification that does not fertility or will not disperse in vector population. Requires acceptability, infrastructure, and money.
Chemoprophylaxis is the use of antimalarial drugs to prevent clinical disease. In
high- transmission areas it is recommended for pregnant women (given at antenatal visits) and infants (given with routine vaccination).
Travellers from the
1
Bite prevention advice: insect repellents with 20– 50
old including pregnant and breast- feeding women). Apply after sunscreen
with
2
Chemoprophylaxis (table
nhs.uk/ desti nati ons.aspx
Table 9.
20
Area Regimen Notes
No drug
resistance
(non- P.
falciparum)
Chloroquineresistant
P. falciparum
UK to malaria areas should be given:
SPF
>30
as DEET may sunscreen ecacy.
Prophylactic regimen against malaria in adults (refer to BNF)
Chloroquine
week PLUS proguanil
200
mg OD
Mefloquine
Doxycycline
Atovaquone- proguanil
combination
Vaccination (RTS,S) is being piloted for children by WHO within selected high- risk
African nations. Results are awaited.
Malaria eradication is the permanent reduction of the incidence of malaria.
Social, demographic, and economic factors, the available healthcare system, and
investment all determine success. Parasitologic (as opposed to clinical) cure is required in order to eliminate asymptomatic transmission.
310
mg base on day 2 and 3. But:
d.
d.
6
PD deficiency so screen prior to use. Seek
G6PD deficiency, and in pregnancy.
3
yrs, a lifespan of 5yrs could save ~$3.8bn. Insecticidal
% DEET (for all >2 months
9.20
) according to area of travel. See www.fitfo rtra vel.
310
mg base/
250
mg/ weekOR2– 3
100
mg OD OR1– 2d prior, 4wks after travel. SE: hep-
1
wk before and 4wks after travel
Chloroquine
CI: epilepsy
Proguanil
if possibility of pregnancy)
Neuropsychiatric
atic impairment, teratogenic
1– 2
advice if taking
: GI disturbance, headache
: diarrhoea, anti- folate (care
wks prior and 4wks after travel
SE, dizziness
d prior, 1wk after travel. Expert
HIV ART
415
9 Infectious diseases
9 Infectious diseases
Mosquito- borne disease
AR
VIRUS
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416
Mosquito- borne diseases13 are transmitted by the bite of a mosquito infected with
a virus, bacteria, or parasite. The mosquito acts as the disease vector. Mosquitoes
are arthropods (see
be described as vector- borne or arthropod- borne disease. When a virus is transmitted by an arthropod it is termed an arbovirus (
Malaria See pp
412– 15
Dengue
Most important arbovirus in humans. Dengue viruses (Flaviviruses
transmitted by day- biting Aedes mosquito.
Symptoms in
Fig 9.
100
mil lion/ yr. UK: ~
January isotherm
10°C
July isotherm
10°C
30
Countries at risk of dengue (dotted line = 10°C isotherm).
Reproduced from Johnson et al., Oxford Handbook of Expedition and Wilderness Medicine,
Presentation Incubation 3– 14d. Febrile phase: fever (up to 40°C), N&V, headache,
retro- orbital pain, myalgia, arthralgia, + ve tourniquet test (inflate
between systolic and diastolic for
critical phase may occur
inal pain, persistent vomiting, fluid accumulation, mucosal bleeding, hepatomegaly,
haematocrit + plts.
severe bleeding, organ involvement (transaminases >
Diagnosis PCR for virus/ ELISA antigen2 during viraemia (~1st 5d of fever).
failure).
IgM, IgG) after
Serology (
Tre at me nt Supportive: prompt but careful fluid balance due to potential for plasma
IV crystalloid, to maintain eective circulation, only in severe disease.
leak.
15– 30
min if hypotensive shock. Monitor clinically and via haematocrit. Reduce
over
IV fluid when stable. Beware: plasma leak maintains haematocrit unless bleeding.
Consider transfusion if haematocrit without clinical improvement. Avoid
Chikungunya
Arbovirus (Alphavirus) transmitted by Aedes mosquito. Widespread: Asia, Africa,
Europe, and Americas. Name derives from Kimakonde language meaning ‘to become contorted’ due to arthralgia. Blood- borne and vertical transmission possible,
Presentation Incubation 1– 12d. Fever. Polyarthralgia: bilateral, sym-
but rare.
metrical, can be severe, persistent. Headache, myalgia,
Diagnosis2 Viral culture/ PCR ( ~1st 8d), serology. Treatment Supportive. Analgesia.
Yellow fever
Arbovirus (Flavivirus) spread by Aedes mosquitoes in Africa, South America.
Presentation Incubation ~3– 6d. Viraemia ~3d with fever, headache, myalgia, anor-
exia,
N&V, relative bradycardia (: enteric fever p
by severe symptoms ~
bleeding. Mortality
3
d.2 Serology: cross reacts with other flaviviruses, IgM can persist after vaccination.
5– 30
Tre at me nt Supportive. Live vaccine, eective for life (certificate for 10yrs).
2
In UK testing done via Rare and Imported Pathogens Laboratory (RIPL): www.gov.uk/ gov ernm ent/ coll ecti ons/
rare- and- impor ted- pathog ens- lab orat ory- ripl
table
9.21
, p
418
). Mosquito- borne diseases can therefore also
thropod- BOrne
).
.
DENV 1–
120
500
countries (fig
imp orted cases/ yr.
5
min≥10 petechiae/ inch2). Warning sign s/
3– 7
d into illness and needs hospital admission: abdom-
9.3 0
), 2.5 billion at risk.
permission from Oxford University Press.
BP cu to midway
4
2016
Severe disease: hypovolaemic shock, respiratory distress,
1000
, GCS, other organ
5
d. Also plts, WCC, transaminitis. (: Chikungunya, Zika.)
20
mL/ kg
NSAIDS.
N&V, maculopapular rash.
411
48
h later: epigastric pain, jaundice, AKI, cardiac instability,
). ~15% have remission followed
%. Diagnosis Clinical and travel history. Virus/ PCR in 1st
) are
, with
Zika virus
https://t.me/med1917
Arbovirus (Flavivirus) transmitted by Aedes mosquito. First identified in Zika
forest, Uganda,
and Brazil (
cases in Americas in
ported cases via blood products.
20
%: fever, conjunctivitis, myalgia, rash. Rarely severe acute illness and Guillain–
~
Barré syndrome.
in first trimester and congenital abnormalities (congenital Zika syndrome, aecting
5– %): microcephaly, intracranial calcification, eye pathology, congenital contrac-
tures. Small study evidence for neonatal mortality.
ELISA
1947
. Human cases rare until outbreak in Pacific Islands (
2015
). Estimated 1.5 million cases in Brazil in
2018
Zika and birth defects Evidence for causality between infection
in blood/ body fluid. Treatment Vector control, avoid non- essential travel
to high- risk areas in pregnancy (see
sexual transmission. Vaccine trials ongoing (
Lymphatic filariasis (elephantiasis)
40
million aected and disfigured.
>
in sub- Saharan Africa). Filarial parasites (nematodes)
transmitted via mosquitoes which bite infected hosts and
ingest microfilaria. These mature in the mosquito with infective larvae transferring to new hosts during feeding.
Adult worms form nests in lymphatic vessels causing
damage and lymphoedema. Transmission prevented by an
annual dose of two drugs—
WHO since
2000
by
• Wuchereria bancrofti (fig
• Brugia malaya ~10%.
• Brugia timori possible cause of disease.
Presentation Asymptomatic infection ± subclinical
.13 Types of filarial worm:
lymphatic damage. Acute episodes of local inflammation: pain, fever. Chronic damage: lymphoedema (
hydrocele, chylocele, scrotal/ penile swelling.
uria, haematuria. Immune hyperreactivitytropical pulmonary eosinophilia (cough, wheeze, fibrosis, eosinophil
IgE). Diagnosis Microfilariae in blood smear
counts,
fig
9.31
), antifilarial IgG, visualization of worms on USS/
(
tissue sample.
in high- risk populations: albendazole plus either
diethylcarbamazine (
cated in onchocerciasis (
loa (
Treatment Lymphoedema care. Prevention
DEC) or ivermectin. DEC is contraindi-
p
435
) due to risk of encephalopathy and renal failure.
Household salt can be fortified with
West Nile and Japanese encephalitis , see ‘Neurological disease’, pp
The global advance of vector- borne disease?
Since
1990
, five species of Aedes mosquito have become established in Europe.
The adaptation of mosquitoes to a temperate environment, combined with future
climate forecasts has led to models
• Plasmodium falciparum transmission by
• Plasmodium vivax transmission by
• Chikungunya transmission in London by
• Dengue transmission after
Of course, modelling is not simple. Socio- economic development, urbanization,
land- use change, migration, and globalization all come into play. Surveillance of
mosquitoes at sea- ports, airports, and used- tyre companies remains uninteresting to date. But consider a time when a visit to South- East England oers an
opportunity to explore the historical gems of our wonderful capital, and simultaneously becomes a pertinent question in your diagnostic sieve.
2016
peak. Fall to 30
. Estimated 1% transmission by sexual contact. Rare re-
Presentation Subclinical in ~80%. Mild illness in
14 Diagnosis PCR of viral RNA/
2007– 2013
www.trav elhe alth pro.org.uk), condoms to prevent
2020
).
900
million at risk (80%
7.7
billion treatments delivered
9.31
) ~90% of disease.
CKD: protein-
p
435
), care with circulating Loa
DEC.
fig
Fig 9.
bancrofti (
Courtesy of Prof S Upton,
9.32
),
Fig 9.
Photo Credit: J. McDowell.
31
Blood smear of W.
290
≈ 8.5µm).
Kansas University.
32
Lymphoedema.
CDC/ Dr. Henry D. Pratt.
432– 3
.
15 that predict the UK will be suitable for:
2030– 2080
.
.
2100
2030
.
2041
.
417
),
000
9 Infectious diseases
9 Infectious diseases
Vector- borne disease
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418
Vector- borne diseases are infections transmitted by the bite of infected arthropod
species including mosquitoes, ticks, flies, and bugs (
Table 9.
21
Vector- borne disease
Vector/ arthropod Disease Page
Mosquito
Anopheles
Aedes
Culex
Ticks Ly me dise ase , ri cket tsia l d isea se, rela psi ng f ever , ti ck-
Bugs/ flies Leishmaniasis, trypanosomiasis, onchocerciasis,
Snails Schistosomiasis
Lym e di sea se (Lyme borreliosis)
Tick - borne multisystem disease due to spirochaete Borrelia
burgdorferi (or related Borrelia spp.). ~All cases limited to nor-
thern hemisphere (mainly Europe and
UK. Risk of infection from tick bite is
yr in
Presentation ≤75% remember tick bite. Needs attachment for
36–48
h for transmission. Disease stages:
• Early localized (3– 30d after bite): erythema migrans (fig
|pain/ pruritus, lymphadenopathy, ± constitutional symptoms:
fever, malaise, headache. ⅓ do not see a rash.
• Early disseminated (w ks– months): borrelial lymphocytoma =
bluish- red plaque/ nodule: check earlobes, nipples, genitals.
Neuroborreliosis: lymphocytic meningitis, ataxia, amnesia,
cranial nerve palsies, neuropathy (severe pain, worse at night),
encephalomyelitis. Carditis: acute- onset
block, myocarditis.
• Late disseminated (months– yr): acrodermatitis chronic atrophicans = focal in-
flammation then atrophic skin; Lyme arthritis.
Diagnosis Clinical: erythema migrans with known exposure or evidence of infection. PCR,
Borrelia culture (sensitivity: <
action with other spirochaete infection:
seroconversion:
3– 15
%. Trea tm en t Erythema migrans: doxycycline
pregnancy). Alternatives: amoxicillin, azithromycin. Neuroborreliosis: ceftriaxone
21
for
Arthritis: doxycycline or ceftriaxone for
IgM
d or doxycycline
1– 2
action due to endotoxins (fever, sweating, malaise); observe
cooling/ antipyretics. Self- resolving
DEET); inspect skin, remove ticks (use tweezers, hold close to head/ mouth).
pellent (
Rickettsial disease
Rickettsiae are obligate, intracellular coccobacillary forms between bacteria and
viruses. Mammals and arthropods are natural hosts. Risk with rural activities.
• Spotted fevers: eg Rocky Mountain spotted fever (Americas), rickettsialpox (
chicken- pox).
• Typhus: scrub typhus in Asia- Pacific regions; endemic (flea- borne) typhus in trop-
ical areas; epidemic (louse- borne) typhus in homeless populations, eg refugees.
• Other emerging illnesses: eg Ehrlichia, Anaplasma.
Presentation Incubation ~1– 2wks. Fever, headache, malaise, rash (maculopapular, ves-
icular, or petechial),
N&V, myalgia. Lymphadenopathy and an eschar at the site of the bite
(scrub typhus). Fulminant, life- threatening infection possible with Rocky Mountain spotted
fever, louse- borne typhus, scrub typhus.
demic area. Serology, culture/
cases: doxycycline, azithromycin, chloramphenicol. Consider permethrin in louse- borne.
3
Specialist diagnostic service and advice in UK via Rare and Imported Pathogens Laboratory (RIPL): www.
gov.uk/ gov ernm ent/ coll ecti ons/ rare- and- impor ted- pathog ens- lab orat ory- ripl
table
9.21
).
Malaria
Dengue, Chikungunya, yellow fever, Zika
Lym phat ic fi lari asis , Ja pan ese e nce phal itis , Wes t Ni le
borne encephalitis, Crimean- Congo haemorrhagic fever
loiasis
US). ~
2000– 3000
cases/
3– 12
% in Europe.
9.33
2
nd/ 3rd- degree heart
20
% for CSF).3 Two- tier serology due to false- positive re-
ELISA + immunoblot. Sensitivity due to slow
412– 15
416
417, 432– 3
418– 19
422– 3,433
419, 435
430
),
Fig 9.
33
Erythema
migrans: distinct advancin g edg e.
Reproduced from
Lewis- Jones, Paediatric
Dermatology
with permission from
Oxford University
– 1
7
,
wks (and may persist), IgG 4– 6wks and background positivity
100
mg BD PO for 21d (CI: <9yrs,
200
mg BD for 21d. Carditis: doxycycline or amoxicillin for 21d.
28
d. Jarisch– Herxheimer Treatment re-
48
h. Prevention Keep limbs covered; use insect re-
1
st ~4h treatment, use
Diagnosis Clinical: fever + ra sh + t ravel to an en-
PCR of blood/ skin biopsy. Tr ea tm en t Antibiotics in severe
2010
Press.
,
Leishmaniasis
HAT
HAT
https://t.me/med1917
Protozoan parasites of Leishmania
by infected female phlebotomine sandflies.
Risk factors: poverty, malnutrition, displacement, deforestation, dam building/ irrigation.
• Cutaneous, most common form, ulceration (fig
• Mucocutaneous (fig
nose, mouth, throat.
• Visceral leishmaniasis (VL, kala- azar, ‘black sickness’) (fig
9.35
): fever, weight loss, hepatosplenomegaly, anaemia.
95
% mortality without treatment. Endemic in Indian
>
9.34
90
subcontinent, East Africa.
Bangladesh, Brazil, Ethiopia, India, South Sudan.
20 000
cases/ yr,
deaths/ yr. Post kala- azar is a complication of Leishmania donovani = a hypopigmented
macular/ nodular rash ( leprosy),
apparent cure, can heal but is a reservoir for parasites
and maintains transmission.
Diagnosis Clinical. Microscopy of tissue (skin, bone
marrow) for parasite. Antibody detection in
fluorescence,
ELISA, western blot, direct agglutination test,
immunochromatographic test) is limited due to:
detectable after cure, cannot distinguish
2
infection.
3
Tests are + ve in many with no history of VL.
Serology may be –ve if HIV + ve. Tre at me nt Liposomal
amphotericin (single dose), oral miltefosine, pentavalent
antimonials (resistance in India).
cases due to
WHO Kala- azar Elimination Programme.
Human African trypanosomiasis (
Infection with Tr yp an os om a p rotoz oan p aras ite s,
Saharan Africa.
• Rhodesiense
95
% reduction in cases since
: incubation <21d, high fever, GI disturbance, lymphadeno pathy,
headache. Chancre at bite site in ~
myopericarditis, arrhythmias, and neurological symptoms.
• Gambiense
tion (can present with acute febrile illness in travellers). Low- grade fever. Sleep
: chronic disease in African population, presents years after infec-
disorder: reversal of sleep– wake cycle, uncontrollable sleep episodes. Weakness,
abnormal gait, psychiatric symptoms.
Diagnosis Hb, plts, AKI, LFTs, polyclonal IgM. Microscopy of parasite (blood,
lymph node, chancre,
CSF). Serology and PCR if available. Treatment According to
disease type and stage. Available from
amidine, nifurtimox- eflornithine. Seek specialist advice— side eects from all.
Chagas’ disease (American trypanosomiasis)
Life- threatening illness due to protozoan Tryp an os om a c ru zi transmitted by
triatomine (kissing) bugs. Endemic in Latin America: ~
Presentation Acute phase (~2 months): skin lesion (chagoma), fever, headache,
myalgia, lymphadenopathy, unilateral conjunctivitis, periorbital oedema (Romaña’s
sign), myocarditis, meningoencephalitis. Chronic phase (yrs): cardiac: dilated cardiomyopathy;
distension, constipation);
CSF, node aspirate. Chronic: serology (Chagas’ IgG ELISA).
GI: mega- oesophagus (dysphagia, aspiration), mega- colon (abdominal
Tre at me nt Benznidazole, nifurtimox. Eectiveness in chronic disease.
Relapsing fever
Caused by spirochaete Borrelia recurrentis (louse- borne, sub- Saharan Africa, refugee
camps) or other Borrelia (tick- borne, worldwide).
‘crisis’ due to antigenic variation (~
BP. Diagnosis Spirochaetes on blood smear, false + ve serology for Lyme disease.
Tre at me nt Doxycycline/ macrolides (single dose if louse- borne). Neuroborreliosis treat-
CNS dis ease ( p
ment if
418
). Jarisch– Herxheimer reaction (p
13 species, transmitted
1
billion at risk.
Presentation
9.5 8
, p
436
).
Fig 9.
34
): leads to tissue destruction of
% occurs in Bolivia, Brazil, Peru.
90
% of new cases occur in
300 000
6
months– 1yr after
VL (indirect
1
Ab levels
VL relapse/ active
75
% reduction in new
HAT,
sle eping sicknes s)
Mucocutaneous
leishmaniasis.
Reproduced with permission
from World Health
Organization. © World
Health Organization.
www.who.int/ leishm ania sis/ muco
cuta neou s_ le ishm ania sis/ en/
Fig 9.
35
Visceral leish-
maniasis.
Reproduced with permission
from World Health
Organization. © World
Health Organization.
www.who.int/ leishm ania sis/
vis cera l_ le ishm ania sis/ en/
http://
http://
16 tra nsm itte d by the t set se fly in s ub-
2000
; <
1000
cas es in
2018
. Includes:
84
%, maculopapular rash. Progresses to
WHO. Includes suramin, melarsoprol, pent-
6– 7
million infected.
CNS symptoms. Diagnosis Acute: trypomastigotes in blood,
CXR
for mega-oesophagus.
Presentation Intermittent fever
3
d fever, then afebrile ~7d), headache, myalgia,
418
) can mimic fever ‘crisis’.
419
9 Infectious diseases
9 Infectious diseases
Zoonoses
https://t.me/med1917
420
Anthrax (Bacillus anthracis)
Gram- positive, aerobic bacillus found in soil worldwide. Humans exposed via infected livestock or animal products, eg hide, wool, tusks. Infection via inhalation,
ingestion, contamination of broken skin (includes
exotoxins: oedema toxin and lethal toxin.
Presentation
• Cutaneous (~95%): itchy papulevesiclenecrotic eschar. Oedema may be striking.
Regional lymphadenopathy, malaise.
• Inhalation: fever, cough, myalgia, SOB, pleural eusion (haemorrhagic mediastin-
itis), stridor, death.
• GI (rare): fever, abdominal pain, ascites, mucosal ulcers, GI perforation.
Diagnosis Vesicular fluid culture (care, do not disseminate), blood culture, antibody
ELISA, PCR. (NB: not pneumonic so sputum cultures are –ve.) Treatment Quinolone/
doxycycline. Two agents if systemic disease, eg ciprofloxacin + clindamycin/linezolid
(then narrow to susceptibility). Consider anti- anthrax monoclonal antibody/ immunoglobulin as adjunct in inhalational disease.
Bartonella
• B. henselae (cat- scratch disease): from infected cat fleas. Low- grade fever, re-
gional lymphadenopathy. Encephalitis rare. Skin lesions mimic Kaposi’s sarcoma.
• B. quintana (trench fever): from human body louse. Fever, headache, bone pain.
• B. bacilliformis (bartonellosis): from infected sandflies in Andes mountains. Oroya
fever = fever, headache, myalgia, haemolysis. Later nodularvascular skin lesions.
Diagnosis Clinical, blood culture (fastidious needs prolonged culture), serology.
Treatment Cat- scratch disease often self- limiting. Azithromycin, aminoglycoside.
Brucellosis
Most common zoonosis worldwide:
swine, goats, sheep, dogs. Human infection via ingestion of infected meat/ unpasteurized milk/ cheese; or through inhalational/ mucosal contact with animal body
fluids (eg farmers, slaughterhouse workers, meat packers, hunters). Risk in
countries without animal health programmes.
sub- acute (
sweats, weight loss, malaise (
itis, meningitis, endocarditis, orchitis, abscess.
incubation due to slow doubling time.
Health England Brucella Reference Unit:
rifampicin, aminoglycoside, co- trimoxazole. Needs prolonged course as intracellular with slow doubling time. Relapse usually due to inadequate dose/ duration/
adherence.
Coxiella burnetii (Q fever)
Q fever is derived from the label ‘query’ fever attributed to an unexplained disease in
Australian abattoir workers. C. burnetii is now recognized as the pathogenic agent.
Sheep, goats, cattle are main sources of infection (also cats, dogs, rabbits, ducks,
ticks). Occurs worldwide. Spores can survive in soil, animal products, and water
for months– yr. Transmitted by contact, inhalation of dust, or consumption of raw
milk products.
atypical, may have rapid progression. Also splenomegaly, granulomatous hepatitis,
aseptic meningitis, encephalitis, osteomyelitis. Endocarditis is the most common
form of chronic disease.
methods.
variation in lipopolysaccharide (
LPS
I LPS. Serology on paired sera
Treatment Doxycycline. Also rifampicin, chloramphenicol, fluoroquinolone, macro-
lide. Hydroxychloroquine alkalinizes the phagosomes in which the bacteria resides
and may bactericidal eect.
1– 6
months), or chronic (>6 months). Non- specific: fever, anorexia,
Presentation Incubation 3– 30d. ~50% asymptomatic. Non- specific
1– 3
17 PCR is rapid. Serology can take
acute infection = IgM/ IgG to phase II LPS, chronic infection = IgG to phase
IV drug use). Bacteria secrete
500 000
cases/ yr. Gram –ve infection of cattle,
Presentation Acute (<1 month),
TB). Localized infection: septic arthritis, spondyl-
Diagnosis Culture with prolonged
17 Serology (four assays performed by Public
0151 529 4900
wks), nausea, fatigue, headache. Pneumonia in 1– 2%: typical or
Diagnosis Coxiella cannot be cultured using routine lab
2– 4
2– 6
LPS) coat. Phase II LPS appears before phase I
wks apart provides best diagnostic evidence.
). Tr ea tm ent Doxycycline,
wks to become positive and detects
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