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Table 2.8 Summary of intestinal diseases caused by helminths (parasitic worms)
Helminth Clinical manifestations Diagnosis Treatment of choice
Large intestine
Water-borne
Food-borne
Whipworm:
Trichuris trichiura
Threadworm:
Enterobius
vermicularis
Trematodes (flukes)
Schistosoma species Parasite eggs, released in urine or faeces, hatch on
Liver flukes
(Clonorchis sinensis,
Opisthorchis
felineus, O. viverrini)
Fasciola hepatica Fever/right upper quadrant pain (RUQ pain)/hepa-
Often asymptomatic. Mucosal damage may result in
bloody diarrhoea
Pruritus ani Apply adhesive paddle
contact with water before infecting freshwater snails.
Snail vectors release cercariae which penetrate
human skin (causing swimmer’s itch). Worms
migrate to pelvic veins and bladder (S. haematobium)
causing haematuria, hydronephrosis, renal failure.
S. mansoni and S. japonicum migrate to mesenteric
veins and bowel causing bloody diarrhoea, intestinal
strictures, hepatic fibrosis and portal hypertension
Cholangitis, biliary carcinoma Eggs on stool
tomegaly
Detection of eggs in
faeces
to perineum and
identify eggs
Detection of eggs in
urine, stool or rectal
biopsy. Serology
microscopy
+ serology
Albendazole/mebendazole
Albendazole/mebendazole
Praziquantel
Praziquantel
Triclabendazole
Fever in the Returned Traveller 33
Continued
34 Infectious diseases
Table 2.8 Summary of intestinal diseases caused by helminths (parasitic worms)
Helminth Clinical manifestations Diagnosis Treatment of choice
Lung fluke
(Paragonimus)
Cestodes (tapeworms)
Taenia saginata Beef tapeworm acquired by eating insufficiently
Taenia solium Pork tapeworm from undercooked pork. Larvae
Echinococcus
granulosus
Chest pain, dyspnoea, fever, cough, haemoptysis Ova on sputum or in
cooked beef. Causes abdominal pain and
malabsorption
penetrate the intestinal wall and cause disseminated
disease involving skin, skeletal muscle and brain
(neurocysticercosis) often presenting with seizure
Hydatid disease acquired by eating meat (from
sheep, cattle) contaminated with ova excreted by
dogs. Large cysts develop in liver, lung and brain.
Anaphylactic reactions if cyst contents escape
—cont'd
stool/serology
Detection of eggs or
proglottids on stool
microscopy
Serology, imaging of
cysts in muscle and
brain by X-ray, CT
or MRI
Ultrasound, CT and
MRI show the cysts
and daughter cysts.
Diagnosis by serology
Praziquantel/triclabendazole
Praziquantel
Albendazole ± praziquantel
(neurological parenchymal
disease requires additional
corticosteroids and antiepileptics)
Surgical excision and albendazole
Miscellaneous Viral Infections 35
MISCELLANEOUS VIRAL INFECTIONS
Zika
Zika virus is a mosquito-borne arbovirus first isolated in the 1940s in Uganda.
The first major outbreak was in 2007 but it came to greater prominence in
2016 following an explosive pandemic throughout South and Central America,
and the Caribbean. Although the illness is mild and self-limiting, causing fever,
rash, headache and myalgia/arthralgia, recent evidence confirms that congenital infection is associated with fetal abnormalities (e.g. Brazil reported a
20-fold increase in the incidence of microcephaly from 2014 to 2015). Precise
data on the magnitude of the risk of congenital brain abnormalities in a Zikaaffected pregnancy are not yet available. The World Health Organization (WHO)
has also concluded that Zika virus is a trigger of the Guillain–Barré syndrome.
Given the now worldwide distribution of other arboviruses, there is significant
concern that Zika virus could spread globally. Diagnosis is by serology and
treatment is supportive. Pregnant women are monitored through pregnancy
with fetal ultrasound. Following clinical illness compatible with Zika or confirmed diagnosis, men are advised to use barrier contraception for 6 months
to avoid sexual transmission through infected semen.
MERS Co-V
Middle East respiratory syndrome coronavirus (MERS-CoV) was first isolated
in 2012 in Saudi Arabia. Since then it has been reported in many countries on
the Arabian Peninsula, with mortality reported around 35%. Camels appear
to be the primary animal host. Case clusters in imported infection strongly
suggests that human-to-human transmission occurs and therefore rigorous
infection control practices must be adhered to if there is epidemiological and
clinical risk for infection. Suspected cases should be discussed immediately
with the local Infectious Diseases team and Health Protection unit as per local
policy. The incubation period is not certain, but up to 14 days is widely used
in the risk assessment of cases. Most patients have presented with severe
pneumonia, ARDS and some with acute kidney injury but mild and asymptomatic infection has been reported. Diagnosis is by PCR of upper or lower
respiratory tract specimens. There is no antiviral treatment available, and full
supportive measures, particularly mechanical ventilation, are often required.
COVID-19
Coronavirus disease-19 (COVID-19) is an infectious disease caused by
severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). It was
first identified in December 2019 in Wuhan, China and subsequently led to
a global pandemic, with cases reported in almost every country worldwide.
nd
36 Infectious diseases
The WHO’s COVID-19 dashboard (http://who.int/emergencies/diseases/novel-
coronavirus-2019) provides up-to-date COVID-19 statistics. At the time of
writing, more than 113 million cases have been recorded, with more than
2.5 million deaths worldwide.
The clinical presentation is that of a respiratory illness with common
symptoms including a fever, persistent cough, loss of taste or smell and
fatigue. In the majority of people, the illness is mild and complete recovery
is expected, but for some, progression to ARDS, multiorgan failure and death
occurs. Transmission occurs through direct or indirect close contact with
infected individuals via infected secretions or respiratory droplets. Less
commonly, transmission via fomites may occur. In the healthcare setting,
airborne transmission may occur during aerosol-generating procedures (e.g.
nebulizers, intubation). Environments where individuals are in close contact
with each other have been associated with widespread transmission of the
virus, e.g. long-term care institutions, factories, cruise ships.
The incubation period is estimated to be around 5 days with patients
being contagious not only whilst symptomatic but also for several days before
the onset of symptoms. Asymptomatic transmission has also been reported.
Diagnosis is by real-time reverse transcriptase polymerase chain reaction
(rRT-PCR) from a nasopharyngeal swab.
The pathophysiology of the illness remains incompletely understood,
but a number of factors have been associated with greater risk of severe
infection including older age, male sex, obesity, ethnicity and the presence
of comorbidities, such as cardiovascular disease, hypertension, diabetes and
chronic respiratory and renal disease. Children and young people comprise only
1%–2% of cases of COVID-19 worldwide and infection in children appears to
be associated with a milder illness than in adults. However, a severe disease
phenotype associated with SARS-CoV-2 has been described with evidence
of a multisystem hyperinflammatory state with features similar to Kawasaki
disease. In adults, severe complications may include pneumonia, ARDS, heart
failure, arrhythmias, thrombotic disorders, multiorgan failure and death.
Treatment is supportive with oxygen therapy, intravenous fluids and, if
required, critical care support of major organ dysfunction. Clinical trials are
underway to investigate the potential benefit of therapeutic interventions.
The RECOVERY trial showed that dexamethasone reduced 28-day mortality
in patients who were receiving invasive mechanical ventilation or oxygen, but
it did not affect mortality in patients who did not need respiratory support.
The REMAP-CAP trial showed that adding interleukin 6 receptor antagonists
(tocilizumab or sarilumab) to dexamethasone therapy within 24h of admission
to an intensive care unit reduced mortality from 35.8% to 27.3%. There is an
ongoing focus on reducing transmission through social distancing, wearing
of face masks, hand hygiene and shielding of patients recognized to be at
increased risk of severe infection. Several countries have active vaccination
programmes in place, but there will be significant logistical challenges to
widespread vaccination on a global scale.
Gastroenteritis and Food Poisoningnd 37
Some people report lasting effects following resolution of infection with SARSCoV-2: so-called ‘long COVID’. Commonly reported symptoms include fatigue,
dyspnoea, arthralgia, chest pain, difficulty performing everyday tasks, anxiety and
depression. There is ongoing research in this area but little is currently known
about management and prognosis for people affected by long COVID.
GASTROENTERITIS AND FOOD POISONING
Most causes of acute diarrhoea (lasting less than 14 days) with or without
vomiting are due to a gastrointestinal infection with bacteria, virus or protozoa.
Not all cases of gastroenteritis are food poisoning, as the pathogens are not
always food- or water-borne, e.g. C. difficile as a complication of antibiotic use
(see below). Individuals at increased risk of infection include infants and young
children, the elderly, travellers (principally to developing countries), the immunocompromised and those with reduced gastric acid secretion (e.g. individuals
using proton pump inhibitors or with pernicious anaemia). Viral gastroenteritis
is a common cause of diarrhoea and vomiting in young children. Helminthic gut
infections are rare in the West but relatively common in developing countries.
Bacteria can cause diarrhoea in three different ways resulting in two
broad clinical syndromes: watery diarrhoea and bloody diarrhoea, i.e.
dysentery (see Table 2.6).
The clinical features based on the principal presenting symptom
associated with the causative organisms of food poisoning are summarized
in Table 2.9. Listeriosis (infection with Listeria monocytogenes) is associated
with contaminated coleslaw, non-pasteurized soft cheeses and other
packaged chilled foods. The most serious complication of listerial infection
is meningitis, occurring perinatally and in immunocompromised adults.
Hepatitis A (p. 146) and Toxoplasma gondii (p. 59) are also acquired from
infected foods and their major effects are extraintestinal.
Most infectious causes of diarrhoea are self-limiting. Routine stool
examination for culture, microscopy for ova and parasites (three samples, since
excretion is intermittent) and stool testing for C. difficile toxin are not usually
necessary other than in the following groups of patients: immunosuppressed,
patients with inflammatory bowel disease (to distinguish a flare from infection),
certain employees, such as food handlers, or patients with bloody diarrhoea,
persistent diarrhoea (>7 days, possible Giardia, Cryptosporidium, Cyclospora),
severe symptoms (fever, volume depletion) or recent antibiotic treatment or
hospitalization. The management of patients with acute diarrhoea primarily
involves adequate hydration. Antibiotic therapy is not given in most cases
since the illness is usually self-limiting. Antibiotics are avoided in patients with
suspected or proven enterohaemorrhagic E. coli infection as they may increase
the risk of haemolytic uraemic syndrome. As a result, the use of empirical
antibiotic therapy (e.g. ciprofloxacin and metronidazole for severely unwell
patients) should be discussed with an infection specialist first.
nd
38 Infectious diseases
Table 2.9 Major food-borne microbes by the principal presenting gastrointestinal symptom in immunocompetent adults
Clinical
presentation
Vomiting
Watery diarrhoea
Organism Source/vehicles Incubation
period
Staph. aureus
Prepared food (e.g.
2–4 h
sandwiches)
Bacillus cereus
Norovirus
Rice, meat
Shellfish, prepared
1–6 h
24–48 h
food
Clostridium perfringens
Enterotoxigenic E. coli (ETEC)
Enteric viruses
Cryptosporidium parvum and
C. hominis
Cyclospora cayetanensis
Yersinia enterocolitica
Vibrio cholerae
All by contaminated
food and water
8–22 h
24 h
Variable
5–28 days
7 days
2–14 h
Hours to
6 days
Diagnosis Recovery
Diagnosis usually
clinical for all organisms
PCR for norovirus
<24 h
2–3 days
2–3 days
available in outbreaks
Stool culture
2–3 days
1–4 days
Variable
7–14 days
Weeks to months
1–22 days
2–3 days
nd
Table 2.9 Major food-borne microbes by the principal presenting gastrointestinal symptom in immunocompetent adults
Diarrhoea with blood
(dysentery)
Campylobacter jejuni
Non-typhoidal salmonella
Enterohaemorrhagic E. coli
Cattle and poultry –
meat and milk
Cattle and poultry –
eggs, meat
Cattle – meat, milk
48–96 h
12–48 h
12–48 h
Stool culture
3–5 days
3–6 days, may be up
to 2 weeks
10–12 days
nd
(usually serotype O157:H7)*
Shigella spp.
Contaminated food
24–48 h
7–10 days
andwater
1–12 days
10–14 days
Variable
Non-gastrointestinal
manifestations
Vibrio parahaemolyticus
Clostridium botulinum
Paralysis due to
neuromuscular blockade
Listeria monocytogenes
Contaminated seafood
Environment – bottled
or canned food
Contaminated
packaged chilled foods
2–48 h
18–24 h
Up to 6 weeks
Toxin in food or faeces
CSF culture
Meningitis
*It is vital that there is low threshold for suspecting E. coli O157 infection in gastroenteritis because it can cause serious complications. Between 1% and 15% of cases progress to
haemolytic uraemic syndrome (acute kidney injury, haemolytic anaemia, thrombocytopenia). Antibiotics are contraindicated in E. coli O157 infection.
Gastroenteritis and Food Poisoning
nd
39
40 Infectious diseases
Clostridium difficile
C. difficile is responsible for some cases of antibiotic-related diarrhoea and
nearly all cases of pseudomembranous colitis. Some patients have recurring
episodes following initial infection.
Pathology and clinical features
C. difficile can be cultured from the stool of 3% of healthy adults and
about one-third of hospital inpatients. Most colonized patients remain
asymptomatic. Clinical disease develops when the normal colonic microbiota is altered, usually by antibiotics, and creates an environment which
favours the proliferation of C. difficile. Infection with toxigenic strains of
C. difficile causes colonic inflammation and diarrhoea by secretion of
toxins A and B. The colonic mucosa is inflamed and ulcerated, and can
be covered by an adherent membrane-like material (pseudomembranous
colitis). The clinical picture varies from mild diarrhoea to life-threatening
severe disease with profuse diarrhoea, abdominal pain and toxic megacolon. Markers of severity include:
• temperature >38.5°C
• white cell count >15 × 10
• serum creatinine >50% above baseline
• raised serum lactate
• severe abdominal pain.
Diagnosis is made by detecting A or B toxins in the stools using enzyme-
linked immunosorbent assay (ELISA) or PCR for C. difficile nucleic acid.
9
Management
Patients with C. difficile-associated diarrhoea should have specific multidisciplinary assessment and input at least weekly. Patients require isolation
with barrier precautions and daily review of severity markers, fluid resuscitation, electrolyte replacement and nutritional status. If at all possible,
ongoing antibiotic treatment should be discontinued, and if the patient is
receiving acid-suppressing medications such as proton pump inhibitors,
these should be stopped if possible. Evidence is increasing that these may
be a risk factor for C. difficile infection.
Antimicrobial approaches depend on the severity of the infection and
whether this is a first episode or recurrence. Certain patient groups, particularly
the elderly and those with multiple comorbidities, are more likely to have severe
disease and recurrent episodes.
Mild/moderate disease is treated with oral metronidazole 500 mg 8 hourly
for 10–14 days. More severe disease is treated with oral vancomycin 125 mg
6 hourly. Some centres now use fidaxomicin in cases that have relapsed
following other treatments. In refractory cases, instilling faeces from the
bowel of a healthy donor (faecal transplant) can restore normal bowel flora
and eradicate the C. difficile infection.
Gastroenteritis and Food Poisoningnd 41
Prevention of C. difficile infection
Prevention of C. difficile infection relies on responsible use of antibiotics
(avoid broad-spectrum agents, use the shortest treatment course likely
to be effective, avoid intravenous antibiotics and use single antibiotic
doses for surgical prophylaxis), meticulous hygiene and isolation of
patients with symptomatic C. difficile infection in hospital or residential
care homes.
Travellers’ diarrhoea
This is one of the most common illnesses in people who travel internationally and affects 20%–50% of travellers depending on destination. The risk
is highest in people travelling to areas with poor food and water hygiene.
Clinical features
The clinical features of travellers’ diarrhoea consist of diarrhoea (with or
without blood), abdominal cramps, fever, nausea and vomiting, which usually resolve without treatment over several days. A prolonged illness lasting
weeks is more likely to be caused by protozoan parasites (see Table 2.9).
Treatment and prevention
To reduce the risk of infection, travellers are advised to drink bottled water,
peel fruit before eating it and avoid salads because the ingredients may have
been washed in contaminated water. Antibiotic prophylaxis with ciprofloxacin
is not indicated for most travellers but is given when an underlying medical
illness would be compromised by diarrhoea, e.g. patients with an ileostomy,
immunosuppression and chronic kidney disease.
Treatment of travellers’ diarrhoea is for the most part symptomatic. Fever
and significant bloody diarrhoea is concerning for amoebic dysentery or
invasive bacterial infection and empirical treatment should be considered
with fluoroquinolones or cephalosporins. Campylobacter isolates are
becoming increasingly fluoroquinolone resistant, especially in Asia, and in
this case azithromycin should be used.
Colonoscopy and biopsy are occasionally necessary in patients with
persistent diarrhoea, when an alternative diagnosis to travellers’ diarrhoea,
such as inflammatory bowel disease, seems likely.
Amoebiasis
Amoebiasis is caused by the protozoal organism Entamoeba histolytica.
Infection occurs worldwide, although much higher incidence rates are
found in the tropics and subtropics. Transmission of infection is by ingestion
of cysts in contaminated food and water or spread directly by person-toperson contact.
nd
42 Infectious diseases
Clinical features
Intestinal amoebiasis (amoebic dysentery)
E. histolytica invades the colonic epithelium, leading to tissue necrosis and
ulceration. Ulceration may deepen and progress under the mucosa to form
typical flask-like ulcers. The presentation varies from mild bloody diarrhoea
to fulminating colitis, with the risk of toxic dilatation, perforation and peritonitis. An amoeboma (inflammatory fibrotic mass) may develop, commonly in
the caecum or rectosigmoid region, which may bleed, cause obstruction or
intussusception, or be mistaken for a carcinoma.
Amoebic liver abscess
An amoebic liver abscess (often single and in right lobe of liver) develops when
organisms invade through the bowel serosa, enter the portal vein and pass into
the liver. The incubation period is 8–20 weeks. There is tender hepatomegaly, a
high swinging fever and profound malaise. There may not be a history of colitis.
Investigations
Serology
Amoebic fluorescent antibody test (FAT) is positive in 90% of patients with
liver abscess and in 60%–70% of patients with active colitis.
Colonic disease
Microscopic examination of fresh stool or colonic exudate obtained at sigmoidoscopy shows the motile trophozoites, which contain red blood cells.
E. histolytica must be distinguished by molecular techniques from the nonpathogenic E. dispar, which appears identical but has no clinical relevance.
Liver disease
Liver abscesses should be considered when liver function testing is abnormal. There may be a raised right hemidiaphragm on chest X-ray. Liver
ultrasonography or CT scan will confirm the presence of an abscess.
Differential diagnosis
Amoebic colitis must be differentiated from the other causes of bloody diarrhoea:
inflammatory bowel disease, bacillary dysentery, E. coli, Campylobacter sp.,
salmonellae and, rarely, pseudomembranous colitis. An amoebic liver abscess
must be differentiated from a pyogenic abscess and/or a hydatid cyst. In patients
with exposure in the Middle East, Central Asia and some parts of Africa, hydatid
disease should be excluded by serological testing (see Table 2.8).
Management
• Colitis – oral metronidazole or tinidazole, followed by a luminal amoebicide
such as diloxanide furoate or paromomycin to clear the bowel of parasites.