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Case 91: A Painful, Swollen Jaw
289
been used for varying periods of time depending on the site of infection, response to treat-
ment, and species of Actinomyces isolated. It is best to discuss each patient with microbiology
or infection specialists.
While antibiotics are the mainstay of treatment, surgery may be needed to remove infected
tissue in cases that do not respond to medical treatment, when extensive sinuses or fistulae
are present, when there is extensive necrosis or abscesses or when malignancy cannot be
excluded.
KEY POINTS
•
Actinomycosis is a chronic, slowly progressive, destructive infection caused by the
anaerobic Gram-positive bacterium Actinomyces sp., most commonly A. israelii.
•
Actinomycosis presents as cervicofacial (most common), thoracic, abdominal, pel-
vic or CNS pathology.
•
Culture of Actinomyces sp. from the clinical specimen is needed to confirm the
diagnosis, which can take up to 3 weeks.
•
Treatment often involves prolonged antibiotic treatment and occasionally surger y.
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CASE 92: TRAVELLER’S DIARRHOEA
A 25-year-old woman presents with a 3-week history of explosive, loose, watery diarrhoea that
started 10 days after she returned from a holiday in Nepal. She drank bottled water while there,
but brushed her teeth with tap water and had ice in her drinks. She opens her bowels at least five
times a day and has increased flatulence. Her stools are foul smelling and float in the toilet bowl.
There is no blood in the stool. The diarrhoea is associated with cramping central abdominal
pain. Her appetite is unchanged, there is no vomiting, but she has noticed some weight loss. Her
past medical history is unremarkable. She does not take any regular medications.
Examination
She is haemodynamically stable and not dehydrated. Her abdomen is slightly distended but
is soft and non-tender to palpation. There is no organomegaly, and the liver is not tender to
palpation. Auscultation reveals normal bowel sounds.
INVESTIGATIONS
Bloods
Haematology and renal and liver function tests are within normal range. Inflammatory
markers are not raised.
Radiology
Abdominal x-ray showed mildly dilated loops of bowel but no evidence of obstruction.
Microbiology
No pathogens isolated from stool MC&S. Stool ova, cysts and parasites (OCP) reveal
multiple cystic structures measuring 10 × 10 micrometres. These are smooth-walled and
oval (
Figure 92.1).
Figure 92.1 Wet mount of stool sample stained with iodine.
QUESTIONS
1. What are the causes of diarrhoea in a returning traveller?
2. What is the diagnosis in this case?
3. How is this treated, and can it be prevented?
DOI: 10.1201/9781003242697-96
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100 Cases in Clinical Pathology and Laboratory Medicine
292
ANSWERS
Travellers’ diarrhoea is an encompassing term of the syndrome of diarrhoea occurring in
travellers. It is the most common health issue aecting returning travellers. It can be caused
by a number of dierent organisms, including bacteria, viruses and parasites. The incuba-
tion period varies by causal agent. Onset of symptoms for viruses and bacteria range from
6 to 24 hours after exposure, whereas intestinal parasites take 1–3 weeks before the onset of
symptoms. Common causes include bacteria such as Escherichia coli (ETEC), Campylobacter
sp. and Salmonella sp., protozoa such as Cryptosporidium and Giardia spp. and viruses such as
norovirus. Less common causes of diarrhoea in travellers include dysentery (Shigella sp.) and
cholera (Vibrio cholera).
Travellers’ diarrhoea is usually acquired through ingesting contaminated food or water. The
travel destination, clinical symptom, and timing of symptoms will assist in determining the
likely underlying pathogen(s). Small bowel infection usually causes watery diarrhoea, while
large bowel invasion presents as dysentery (bloody diarrhoea) or colitis.
Given the chronic nature of the watery diarrhoea and the travel history in this case, the
cause is more likely parasitic. The dierential diagnosis would include giardiasis, or if
immunocompromised, cryptosporidiosis. More than one pathogen may be associated with
travellers’ diarrhoea, and a full investigation for bacteria, parasites and viruses should be
performed.
The patient’s stool sample (Figure 92.1) contains cysts of Giardia lamblia. Bacterial culture is
negative. This microbiological diagnosis fits with the clinical picture of watery diarrhoea,
foul-smelling steatorrhea (fatty, floating stools) and abdominal cramps. Giardia is most
prevalent in developing countries on account of poor sanitation. However, it also occurs in
developed countries where water treatment is not adequate. G. lamblia is a protozoan para-
site acquired from ingestion of cysts in contaminated water or food or by the faecal-oral
route. Once in the small intestine they excyst, releasing trophozoites that bind to the small
intestinal wall. Here they cause damage leading to reduced absorption of solutes, which
causes an osmotic diarrhoea and malabsorption of fat and fat-soluble vitamins, resulting in
steatorrhea.
Diagnosis is by stool microscopy looking for ova, cysts, and parasites. This should be requested
on all patients with travellers’ diarrhoea even if another pathogen is isolated, as multiple
infections may occur. The cyst and trophozoite stages are both seen in the stool and will be
detected in 90% of cases if stool samples are collected on 3 separate days.
Several drugs can treat giardiasis, including albendazole, tinidazole and metronidazole. The
close contacts of the patient should also be screened for giardiasis.
There is no vaccine against giardiasis. Prevention of giardiasis, and other causes of travel-
lers’ diarrhoea, is best done using good food and water hygiene practices. Avoid drinking
tap water or using it to brush teeth or make ice. If this is not possible, boil or treat the
water before use. Drinking bottled or tinned water and drinks is preferred. Eating hot,
well-cooked food and avoiding street food, undercooked food or food that has been left
standing will reduce the risk. Avoid raw foods such as salads or unwashed fruits. Washing
your hands before eating is essential, which can be done using soap and water or alcohol-
based hand gels.
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Case 92: Traveller’s Diarrhoea
293
KEY POINTS
•
Travellers’ diarrhoea can be caused by one (or more) of a number of different
organisms, including bacteria, parasites and viruses.
•
G. lamblia is a protozoan parasite acquired from ingestion of cysts in contami-
nated water or food or by the faecal-oral route. Giardia is most prevalent in devel-
oping countries on account of poor sanitation.
•
Giardiasis has a clinical picture of chronic watery diarrhoea, steatorrhea, and
abdominal cramps, together with anorexia and weight loss.
•
The cyst and trophozoite stages are both seen in the stool and will be detected in
90% of cases if three stool samples are collected on different days.
•
Prevention of infection when travelling is best achieved through good food and
water precautions.
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CASE 93: FEVER IN A RETURNING TRAVELLER
A 27-year-old Ghanaian woman presents to the emergency department with a 3-day history
of rigors, headache, nausea and vague lower abdominal pain. She has no significant past
medical history, but is 8 weeks pregnant with her first child. She is in a monogamous relation-
ship and denies any risky sexual contact or drug use. She lives in London and returned from
a trip to Ghana 1 week ago.
She did not take malaria prophylaxis, as she is pregnant and was staying with her family in
the city. She doesn’t recall any bites, but was aware of the presence of mosquitoes in the envi-
ronment. She ate food prepared by her mother or other family members on most occasions,
although she did eat at some local take-away restaurants. She is not aware of anyone else in her
household being similarly ill. She had no history of rash, joint pains, diarrhoea, jaundice, dysuria
or respiratory symptoms. She does have urinary frequency that she put down to her pregnancy.
Examination
Temperature 39.8°C, blood pressure 99/60 mmHg, pulse 142 beats/min. There was no rash,
no petechiae, no jaundice and no lymphadenopathy. There was no evidence of either mos-
quito or tick bites. Her ear/nose/throat (ENT) examination was normal.
General examination revealed some lower abdominal tenderness with some guarding. The uterus
was not palpable. There is no evidence of hepatosplenomegaly or other masses in the abdomen.
Respiratory and cardiovascular examinations were unremarkable aside from the tachycardia.
INVESTIGATIONS
Bloods
Haemoglobin 8.8 g/dL
White cell count 2.95 × 109/L
Platelets 41 × 109/L
Urea 8.4 mmol/L
Creatinine 178 mol/L
Blood glucose 3.8 mmol/L
Bilirubin 72 mol/L
Alanine aminotransferase 31 IU/L
Aspartate aminotransferase 38 IU/L
Lactate dehydrogenase 500 IU/L
C-reactive protein 82 mg/L
QUESTIONS
1. Based on the clinical findings, what is your differential diagnosis?
2. Give a possible explanation of the abnormal blood results and use this together
with the clinical picture to explain what additional specimens and tests you
would request. What is the most likely diagnosis?
3. How may pregnancy complicate this case?
4. What is the appropriate treatment?
DOI: 10.1201/9781003242697-97
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100 Cases in Clinical Pathology and Laboratory Medicine
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ANSWERS
Given the symptoms, signs, results and travel history, it is crucial to consider both travel-
related and non-travel-related infections. In this case malaria, typhoid, hepatitis, dengue,
yellow fever, schistosomiasis, SARS-CoV-2 and meningococcal disease should be considered
in the dierential diagnosis, as well as a urinary tract infection (UTI). Acute HIV serocon-
version illness should always be considered as a dierential in sexually active people.
Relevant investigations include:
•
Full blood count and clotting screen, as bleeding can occur in the haemorrhagic
fevers (dengue and yellow fever), meningococcal sepsis, malaria (owing to low plate-
lets) and hepatitis (if severe liver dysfunction occurs).
•
Liver function tests, as jaundice may occur in malaria, typhoid, hepatitis, dengue,
yellow fever, schistosomiasis and meningococcal disease if there is severe sepsis.
•
Abdominal pain and tenderness, fever, nausea, raised bilirubin and abnormal liver
function tests require hepatitis studies.
Further specimens and tests suggested include:
•
Urine microscopy, culture, and sensitivity (MC&S) for lower abdominal pain, fever
and frequency to rule out a UTI.
•
COVID-19 reverse transcription polymerase chain reaction (RT-PCR) test
•
Travel plus fever requires blood cultures to exclude typhoid (abdominal pain,
endemic area, fever, low platelets, low white blood cells) and meningococcal disease
(endemic area, fever, low platelets).
•
Abdominal pain and tenderness, anaemia and raised bilirubin require a stool sam-
ple for bacterial, viral, and parasitic pathogens.
•
Travel to endemic area associated with fever, low platelets, low white blood cells
and a raised LDH necessitate a malaria film. In this case microscopy of thick and
thin blood smear (Figure 93.1) displays multiple ring-form trophozoites inhabiting
a single, normal-sized erythrocyte, consistent with Plasmodium falciparum infection.
•
Serum analysis for dengue was negative but is an important test because of the
endemic area, fever, low platelets and low white blood cells.
Figure 93.1 Blood smear of a P. falciparum culture (K1 strain). Ring stages on right and top
left, including multiple rings in one red blood cell, schizont in the lower centre, trophozoite
on the left.
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Case 93: Fever in a Returning Traveller
297
Malaria is an acute febrile illness. In a non-immune individual, symptoms appear 7 days
or more (usually 10–15 days) after the mosquito bite. The first symptoms—fever, headache,
chills and vomiting—may be mild and dicult to recognise as malaria. If not treated within
24 hours, P. falciparum malaria can progress to severe illness often leading to death.
Worldwide malaria infects approximately 250 million and kills approximately 1 million
people per year. Rising temperatures and changing weather patterns are expected to expand
the burden of this disease. The majority of infection occurs in young children living in the
tropics (mainly sub-Saharan Africa, Middle East, India and South America), with the most
deaths occurring in sub-Saharan Africa. Five Plasmodium species cause malaria in humans.
P. falciparum and P. vivax are the most common, with P. falciparum being the deadliest. The
others are P. malariae, P. ovale and P. knowlesi. Five per cent of patients are infected with more
than one species. For P. vivax and P. ovale relapses can occur weeks to months after the primary
infection, as they have an inactive hypnozoite stage in the hepatocytes which can reactivate.
Transmission of the parasite occurs when the female Anopheles mosquito bites a human,
releasing sporozoites from its salivary glands into the blood. These sporozoites enter hepa-
tocytes where they incubate for 2–3 weeks. During this time they reproduce asexually to
produce merozoites. Eventually the hepatocytes burst, releasing a mass of merozoites that
rapidly invade erythrocytes, where further replication and release take place. Every 48–72
hours, the erythrocytes burst to logarithmically increase the parasite burden. Clinically, this
correlates with a peak in fever every 48–72 hours, known as periodicity. This periodic fever
often alternates with feeling cold and shivering. This process can result in severe anaemia.
Pathologically, erythrocytes infected with P. falciparum are able to adhere to and block the
post-capillary blood vessels of several organs. This process can result in cerebral malaria
and multi-system end-organ failure. Other complications of persistently high parasitaemia
include blackwater fever (haemoglobinuria), which is a result of severe red cell destruction
that produces dark urine with renal failure.
Malaria is more frequent and more complicated during pregnancy, especially in a first preg-
nancy. There is increased risk of maternal anaemia, respiratory complications and death
from severe malaria. Miscarriage, stillbirth and intrauterine growth restriction are com-
plications of maternal anaemia and placental infection. Prophylaxis and treatment in preg-
nancy are also more complicated, as some of the drugs used are contraindicated, owing to
insucient safety data or because they cause severe side eects.
Urgent treatment is necessary with expert advice. The first-line treatment of pregnant women
is quinine. Hypoglycaemia, a complication of both quinine and the malarial parasite, is more
common in pregnant women. Neither Coartem nor atovaquone-proguanil is recommended
for use during pregnancy in the UK. Doxycycline is always contraindicated in pregnancy,
and clindamycin should be used as a second drug together with quinine.
KEY POINTS
•
P. falciparum is the most virulent species of human malaria.
•
Malaria often presents with fever and non-specific symptoms and should always
be considered in a traveller returning from a high-risk area.
•
A thick blood film is best for screening and a thin blood film for species identifica-
tion. Characteristically P. falciparum demonstrates a signet ring–shaped parasite
surrounded by a thin cytoplasm ring. Multiple ring forms in a single erythrocyte is
also characteristic.
•
Malaria infection is potentially fatal and should be treated urgently with expert input.
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