Добавил:
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_3120_Библиотеки_им_академика_М_И_Перельмана

.pdf
Скачиваний:
0
Добавлен:
12.10.2026
Размер:
5 Мб
Скачать
☆
Case 96: A Chronic Cough
309
TB can cause a disseminated illness and is not necessarily confined to the respiratory tract.
Other presentations of TB include lymphadenitis, meningitis, bone and joint infections and
gastrointestinal and genitourinary tract infections. Microbiological samples should be taken
from appropriate sites.
TB is spread from person to person through the air. When a person with infectious pulmo-
nary TB coughs or sneezes, tiny particles containing Mycobacterium tuberculosis are expelled.
These particles, called droplet nuclei, are about 1–5 microns in diameter and can remain
suspended in the air for several hours. If another person inhales air that contains these drop-
let nuclei, they reach the alveoli, and transmission of infection may occur. Not everyone who
is exposed to an infectious TB patient becomes infected. The risk depends on how infectious
the patient is, the duration of exposure, the virulence of the TB strain and the immune status
of the contact person.
In the alveoli, some of the tubercle bacilli are killed, but a few multiply and disseminate.
Bacilli may reach any part of the body, including areas where disease is likely to develop,
such as upper portions of the lungs, kidneys, brain and bone. The spread and multiplication
are stopped within 2–8 weeks by the body’s immune response. At this time, the person has
what is known as latent TB infection (LTBI). LTBI means that bacilli are in the body but the
immune system is keeping them under control and inactive.
Some people with LTBI develop TB disease. TB disease develops when the immune system
cannot keep the bacilli under control and they begin to multiply rapidly. The risk of develop-
ing TB disease is highest in the first 2 years after infection.
If active PTB is suspected and the patient is very unwell, treatment should be commenced
without waiting for the culture results. Once a diagnosis is made, the patient should be
transferred to the care of a physician with experience managing pulmonary TB. If hospital
admission is needed, patients should be admitted to a single isolation room under respira-
tory precautions, and if suspicion of drug-resistant TB exists, they should be admitted to a
negative-pressure side room. This is to reduce the spread of infection to others. All patients
with TB should have an HIV test performed. All close contacts should be screened to see if
transmission has occurred.
The standard treatment regimen comprises quadruple therapy with rifampicin, isoniazid,
ethambutol and pyrazinamide. Pyrazinamide and ethambutol are stopped after 2 months
and rifampicin and isoniazid continued for a further 4 months, to complete 6 months in total
of treatment for PTB. Treatment with multiple drugs is used to reduce the development of
resistance in the TB bacillus during treatment. TB should never be treated with only one
antibiotic.
https://t.me/medicina_free
100 Cases in Clinical Pathology and Laboratory Medicine
310
KEY POINTS
•
PTB commonly presents as the trio of chronic cough, night sweats and weight loss.
•
Diagnosis is based on clinical suspicion, typical changes on a chest x-ray and a
positive AFB microscopy on respiratory (or other clinical) samples. The gold stan-
dard for diagnosis is culturing the causative organism.
•
TB is spread from person to person through the air by TB-containing particles,
called droplet nuclei. Not everyone who is exposed to an infectious TB patient
becomes infected.
•
If hospital admission is needed, patients should be admitted to a single isolation
room under respiratory precautions.
•
Standard treatment is quadruple therapy initially. Treatment with multiple drugs is
used to reduce the development of resistance in the TB bacillus during treatment.
https://t.me/medicina_free
CASE 97: A JAUNDICED VIEW
A 31-year-old known intravenous drug user (IVDU) is admitted to hospital after a presumed
drug overdose. There is no history available from the patient, and she has no medical records
at this hospital.
Examination
Her Glasgow Coma Scale (GCS) is 12, but there is no meningism or localising signs. She is
haemodynamically stable with a blood pressure of 105/70 mmHg. She has poor oral hygiene
and is missing most of her teeth. She has a number of tattoos, some of which looked self-
made. Her arms are covered in needle track marks. There is no evidence of trauma.
Her abdomen is soft and mildly tender in the right upper quadrant. The rest of the examina-
tion is within normal limits.
INVESTIGATIONS
Bloods
Reference values
Haemoglobin 10.8 g/dL 11.4–15.0 g/dL
White cell count
13.5 × 10
9
/L
3.9–10.6 g/dL
Platelets
408 × 10
9
/L 150–440 × 10
9
/L
Urea 2.1 mmol/L 2.5–7.8 mmol/L
Creatinine 98 mol/L 45–90 mol/l
Bilirubin 46 mol/L <21 mol/L
ALT 270 IU/L <40 IU/L
AST 170 IU/L 5–40 IU/L
ALP 80 IU/L 40–129 IU/L
C-reactive protein 25 mg/L <5 mg/L
Virology
HIV Negative
Hepatitis B sAg (HBsAg) Positive
Hepatitis B sAb (anti-HBs) Negative
Hepatitis B core IgM (anti-IgM) Negative
Hepatitis B core total Ab (anti-HBc) Positive
Hepatitis B eAg (HBeAg) Negative
Hepatitis B eAb (anti-HBe) Positive
Hepatitis C IgG Negative
Radiology
CT brain showed no abnormalities.
QUESTIONS
1. How would you interpret the results?
2. How would you manage this patient?
3. How could this infection have been prevented?
DOI: 10.1201/9781003242697-101
311
https://t.me/medicina_free
100 Cases in Clinical Pathology and Laboratory Medicine
312
ANSWERS
Patients with a history of IVDU are at risk of acquiring blood-borne viruses and should be
investigated for HIV and viral hepatitis.
This patient’s results show mildly elevated ALT, AST, and bilirubin and a normal ALP.
This suggests hepatocyte damage rather than an obstructive jaundice. The enzymes are only
mildly raised, suggesting a chronic rather than acute hepatic process.
Viral serology testing excludes HIV and hepatitis C infection but confirms the presence of
hepatitis B infection. Hepatitis B infection is spread parenterally, sexually and vertically. It
has an incubation period of approximately 3 months, after which the symptoms of acute
hepatitis occur. In the majority of cases this is cleared by the immune system. In 5–10%
of infected persons, failure to clear the virus occurs and a chronic infectious state ensues.
Hepatitis B infection is also causally associated with hepatocellular carcinoma. Hepatitis C
virus is a widely spread RNA virus with similar transmission routes to hepatitis B, although
mainly spread parenterally through blood in transfusions (before screening) and needle shar-
ing (tattoos, IVDU). Patients with hepatitis C are more prone to developing a chronic infec-
tion and cirrhosis than those infected with other forms of hepatitis.
Serological markers are the mainstay of diagnosis of viral hepatitis (Figures 97.1 and 97.2).
After acute infection, the first marker to appear in the blood is hepatitis B surface antigen
(HBsAg), and looking for this antigen is the initial test done when screening for hepatitis B
infection. It is part of the surface protein and reflects the presence of the virus in the blood. It
is positive in acute and chronic infection and only becomes negative if the infection is cleared.
If it is positive for longer than 6 months, the infection is classed as a chronic infection.
Anti-HBs, an antibody to this surface antigen, is produced as the HBsAg wanes. It repre-
sents late acute infection or past infection and the clearance of surface antigen. Positive anti-
HBs can also represent vaccination, as hepatitis B vaccine contains recombinant HBsAg. In
chronic infection, when HBsAg remains positive, anti-HBs will not be produced.
The nucleocapsid of the virus is reflected in two antigens, HBcAg and HBeAg.
Core antigen (HBcAg) is not measurable, as it remains inside the virus, but both IgM (anti-
IgM) and IgG (anti-HBc) antibodies to HBcAg are produced and can be measured. As with
other infections, IgM is produced during acute infection and will also remain positive in
chronic active hepatitis, as the virus is still present. It will disappear once core antigen is no
longer present, that is, once the virus has been cleared. IgG, on the other hand (as with other
infections), will be produced throughout infection and remain positive after recovery as a
marker of previous infection. IgG antibodies therefore do not distinguish between recent,
chronic, or previous infection. If negative, however, they exclude hepatitis B infection.
HBeAg, which is a soluble part of the core antigen, can leave the virus and can therefore be
measured. Its presence reflects actively replicating virus, and it will disappear when the virus
stops replicating. A positive result therefore indicates acute infection or chronic active infec-
tion, implying actively replicating virus and thus high infectivity. Analogous to anti-HBs and
HBsAg, anti-HBe is produced as HBeAg wanes and reflects the ceasing of active viral rep-
lication. A positive result for anti-HBe represents previous infection, or chronic, non-active
hepatitis B.
https://t.me/medicina_free
313
Case 97: A Jaundiced View
HBV DNA
Total anti-HB core
IgM anti-core
Anti-HBs
Anti-HBe
HBsAg
HBeAg
Levels in the blood
0 5 10 months 15
Figure 97.1 Hepatitis B viral antigens and antibodies detectable in the blood following
acute infection and resolution.
Infectivity
HBeAg
anti-HBe
Total anti-HBc
IgM anti-HBc
HBsAg
0 4 8 12 16 20 24 28 32 36
52
Levels HBV antigens and antibodies
in the blood
Weeks after infection
Years after infection
Figure 97.2 Hepatitis B viral antigens and antibodies detectable in the blood following
acute infection which becomes chronic.
This patient’s results therefore suggest a chronic, non-active hepatitis B infection, also known
as a carrier state. A viral polymerase chain reaction (PCR) for hepatitis B virus (HBV) DNA
should be done in all chronic infections to evaluate for viral replication. A liver biopsy should
be considered in chronic hepatitis with a positive HBV DNA.
The other hepatitis viruses include hepatitis A–E and G (GB-V). Despite their structural dif-
ferences and modes of transmission, they all target the liver cells. The vowels (A and E) are
transmitted via the faecal-oral route, are usually associated with travel, and cause an acute
infection presenting as gastroenteritis and hepatitis. They do not cause any chronic disease.
Most patients with hepatitis B will resolve their infection without any specific treatment.
Patients in whom treatment is recommended include those who have evidence of viral repli-
cation. Treatment options currently include interferon and antiviral agents. Patient education
https://t.me/medicina_free
100 Cases in Clinical Pathology and Laboratory Medicine
314
is very important, as prevention of transmission to other people can be achieved only by col-
laboration with the patient.
Prevention of infection is best achieved through vaccination, which is recommended for all
at risk, such as health care workers, emergency service workers, IVDUs, household members
of carriers, post-exposure prophylaxis if non-immune, travellers to high-risk areas and those
on renal dialysis. The vaccine contains the HBsAg and is prepared by recombinant DNA
technology. It is usually given in three doses over a period of 6 months; however, this can be
expedited to 2 months for patients at high risk of infection. It is important to test for serocon-
version after vaccination, as some people do not produce antibodies and are therefore not
protected.
KEY POINTS
•
Intravenous drug users are at risk of acquiring blood-borne viruses and should be
investigated for HIV and viral hepatitis.
•
Hepatitis B is spread parenterally, sexually and vertically. It has an incubation
period of approximately 3 months, after which the symptoms occur.
•
HBsAg is the first marker to appear after acute infection and the first test done
when screening for hepatitis B. Anti-HBs appears in late acute infection and
remains positive. It can also represent immunity from vaccination as the hepatitis
B vaccine contains recombinant HBsAg.
•
Most patients with hepatitis B will resolve their infection without any specific treat-
ment. In 5–10% of infected persons, failure of clearance of the virus occurs and a
chronic state ensues. It is also causally associated with hepatocellular carcinoma.
•
Prevention of infection is best achieved through vaccination, which is recom-
mended for all at risk.
https://t.me/medicina_free
CASE 98: GRAM-NEGATIVE BACTERAEMIA
A 29-year-old man presents to the emergency department complaining of fever, headache,
and malaise over the past couple of days. His symptoms are associated with nausea and
abdominal pain but no diarrhoea. He has no dysuria, haematuria, or frequency and has not
noticed any rash. He returned 4 days ago from a trip to Bangladesh, where he was visiting
family. He noticed some mosquito bites and ate at a lot of fast-food restaurants during his stay.
He has no other significant medical history and is usually fit and well.
Examination
His temperature is 39.5°C, blood pressure 130/80 mmHg and heart rate 70 beats/min.
There is no rash. He has inflamed tonsils, but no spots or rash on the mucous membranes.
His chest is clear. His abdomen is slightly tender, but no masses or organomegaly is found.
It was felt that he was not very unwell, and so he was discharged from the emergency depart-
ment on oral co-amoxiclav after bloods were taken.
INVESTIGATIONS
Bloods Reference values
Haemoglobin 14.8 g/dL 11.4–15.0 g/dL
White cell count
5.1 × 10
9
/L
3.9–10.6 g/dL
Platelets
102 × 10
9
/L 150–440 × 10
9
/L
Urea 5.3 mmol/L 2.5–7.8 mmol/L
Creatinine 89 mol/L 45–90 mol/l
Bilirubin 27 mol/L <21 mol/L
ALT 67 IU/L <40 IU/L
ALP 69 IU/L 40–129 IU/L
C-reactive protein 100 mg/L <5 mg/L
Blood film No malaria
parasites seen
ICT for malaria (antigen test) Negative
Microbiology
1. Blood cultures after 24 hours flagged up positive. Gram stain showed Gram-negative rods.
2. Urine MC&S: Negative.
QUESTIONS
1. What is your differential diagnosis based on the above findings?
2. What would be your management plan?
3. What is the pathogenesis of this infection?
4. What further tests and investigations would you request on this patient?
DOI: 10.1201/97810 03242697-102
315
https://t.me/medicina_free
100 Cases in Clinical Pathology and Laboratory Medicine
316
ANSWERS
In a returning traveller from Bangladesh presenting with a fever, malaria, typhoid fever,
other food-borne pathogens, dengue, arboviruses and hepatitis should be considered. HIV
should also be considered if risk is established. It is important to remember non-travel-related
common infections, such as urinary tract infection, inflammatory bowel disease and chole-
cystitis, that might present similarly.
The blood culture result narrows the diagnosis to conditions caused by a Gram-negative bac-
teraemia. From this, typhoid and paratyphoid are most likely, but it could still be a common
pathogen such as Escherichia coli secondary to a non-travel-related cause.
Enteric fever (sometimes known as typhoid fever) is caused by the Gram-negative pathogens
Salmonella enterica serotypes Typhi and Paratyphi. Transmission of the infection is via the fae-
cal-oral route, and the disease is more common in areas where water, food and hand hygiene
are poor. Humans are the only known reservoir for S. enterica Typhi and S. enterica Paratyphi.
It presents in young adults with a high-grade fever, abdominal pain, and a relative bradycar-
dia, as is seen in this patient. One would expect a faster heart rate with such a high tempera-
ture; however, this is not the case in this patient. In addition, patients usually present with a
relatively low or a normal white cell and platelet count. Impaired liver function tests are also
a common finding.
While uncommon, severe complications can occur. These include intestinal haemorrhage
from congested Peyer’s patches, intestinal perforation, encephalitis, neuropsychiatric symp-
toms and metastatic abscesses.
Patients who are suspected of having typhoid fever should be started on antibiotics, which
can be oral or intravenous depending on their clinical condition. Prior to commencing ther-
apy, however, blood and stool cultures should be sent to the microbiology laboratory. Initial
choice of therapy depends on the susceptibility patterns of the pathogen in the area it was
acquired, as some geographic regions have high resistance to certain antibiotics. Intravenous
ceftriaxone is currently the treatment of choice. Oral options for treatment include cipro-
floxacin and azithromycin, but should be prescribed only once testing has confirmed they are
sensitive. The duration of treatment varies from 7 to 14 days.
The fever usually resolves within 4 days of appropriate therapy, but may last longer. Prolonged
fever is not necessarily a sign of complicated disease.
As salmonellae are highly infectious, all patients should be admitted to an isolation room
and enteric precautions undertaken to prevent spread of the infection to other patients.
Health authorities responsible for public health and epidemiology, such as the Public Health
England, should be notified.
Following ingestion, the organism reaches the intestinal mucosa, where it attaches to the M
cells of the Peyer’s patches, which have a wide array of molecules that assist in the attachment
and invasion of the intestinal barrier. The organism causes systemic infection by crossing
the gastrointestinal epithelial barrier to invade the macrophages at the submucosal space.
Despite the hostile environment within the macrophage, they are able to survive and rep-
licate. The inflammatory response mounted by the host is partially due to activation of the
innate immune response.
A small number of people, called carriers, recover from typhoid fever but continue to carry
the bacteria. Both ill persons and carriers shed Salmonella Typhi in their faeces (stool). Stool
https://t.me/medicina_free
Case 98: Gram-negative Bacteraemia
317
should be tested to ensure clearance of carriage, especially in those working as food handlers
or with vulnerable groups of people.
This patient could have benefited from vaccination prior to travel. Two types of vaccines
are currently available for typhoid: a live oral attenuated vaccine and a parenteral polysac-
charide vaccine. They protect only against S. Typhi and not against S. Paratyphi, so food
hygiene precautions also should be recommended to all travellers to endemic areas.
KEY POINTS
•
Typhoid fever (also known as enteric fever) is caused by the Gram-negative patho-
gens S. enterica serotypes Typhi and Paratyphi. Transmission of the infection is via
the faecal-oral route.
•
Typhoid fever usually presents in young adults with a high-grade fever and non-
specific symptoms.
•
Initial choice of therapy depends on the susceptibility patterns of the pathogen
in the area it was acquired. Intravenous ceftriaxone is currently the treatment of
choice.
•
Both ill persons and carriers shed Salmonella Typhi in their faeces. Thus testing is
important in those working as food handlers or health care professionals.
https://t.me/medicina_free
https://t.me/medicina_free