Fever is an elevated core body temperature that can be caused by infections or non-infectious conditions. It results from cytokines and acute phase proteins. There are various types of fever defined by temperature patterns. Fever causes systemic responses like increased heart rate and metabolic rate. Investigations aim to identify the cause through tests of blood, urine, sputum and imaging. Management involves treating the underlying cause, using paracetamol to reduce fever and its symptoms, and replacing fluids. Sepsis is a serious condition where signs of infection and inflammation affect the whole body. It requires prompt identification of the infection source and aggressive treatment including antibiotics and fluid resuscitation.

2. Fever:
• Elevated core body temperature of more than
38.0°C.
• Is a response to cytokines and acute phase
proteins and occurs in infections and in non-
infectious conditions.
• Recording of Temperature:
• Oral.
• Axillary.
• Rectal.
• Tympanic.

3. • Systemic Responses in Fever:
• Increase in metabolic rate.
• Increase in heart rate.
• Blood pressure.
• Fluid loss increases.
• Increase in respiratory rate.
• Chills occur.
• Headache.
• Delirium.
• Excessive sweating.
• Muscle pain.
• Herpes labialis.
• Feverishness.

4. • Types of fever:
A. Continuous Fever: Temperature is persistently elevated
with diurnal variation of less than 1 C e.g. Typhoid in the
2nd week, typhus, viral infections and others.
B. Remittent Fever – Temperature is persistently elevated
with diurnal variation more than 1oC – typhoid in 1st
week, brucellosis, leptospirosis and others.
C. Intermittent Fever – Temperature is discontinuous,
touching normal at least once in 24 hours. This may be
seen in pyogenic infections, lymphomas, tuberculosis,
bacteremias, malaria and others.
D. Periodic Fever: These show a regular periodicity in their
occurrence. Fever occurring on alternate days with one
day interval in between is called tertian periodicity e.g.
vivax malaria (benign tertian).

5. • Investigations:
1. Full blood count (FBC) with differential. including eosinophil count.
2. Urea and electrolytes, liver function tests (LFTs), blood glucose and
muscle enzymes.
3. Inflammatory markers, erythrocyte sedimentation rate (ESR) and C-
reactive protein (CRP).
4. Test for antibodies to HIV-1.
5. Autoantibodies, including antinuclear antibodies (ANA).
6. Chest X-ray and electrocardiogram (ECG).
7. Urinalysis and urine culture.
8. Blood culture.
9. Throat swab for culture or polymerase chain reaction (PCR).
10. Wound swab; sputum culture; stool culture, microscopy for ova and
parasites.
11. Clostridium difficile toxin assay
12. Malaria test.
13. Abdominal ultrasound.

6. • Management:
a) Treat underlying cause.
b) Give paracetamol for Fever and its associated
systemic symptoms.
c) Tepid sponging to cool the skin.
d) Replacement of salt and water.

7. Fever with localizing symptoms or signs:
• In most patients, the site of infection is apparent after
clinical evaluation.
• Not all apparently localising symptoms are reliable (e.g.
headache, breathlessness and diarrhoea can occur in
sepsis or malaria without localised infection in the central
nervous system (CNS), respiratory tract or gastrointestinal
tract).
• Careful interpretation of the clinical features is vital (e.g.
Severe headache associated with photophobia, rash and
neck stiffness suggests meningitis, whereas moderate
headache with cough and rhinorrhoea is consistent with a
viral upper respiratory tract infection).

9. Pyrexia of unknown origin:
• A temperature above 38.0°C on multiple occasions for
more than 3 weeks, without diagnosis, despite initial
investigation in hospital for 1 week “investigation over 3
days of inpatient care, three outpatient visits”.
• HIV-1 related, immune-deficient or nosocomial.

10. • Clinical assessment:
• Detailed history and examination should be
repeated at regular intervals.
• Causes of PUO:
1. Infections (~30%).
2. Malignancy (~20%).
3. Connective tissue disorders (~15%).
4. Miscellaneous (~20%).
5. Idiopathic (~15%).

12. • Investigations:
• If initial investigation of fever is negative, further
microbiological and non-microbiological
investigations.
1. Induced sputum or other specimens for
mycobacterial stains and culture.
2. Serological tests, including an HIV test, and ferritin
estimation.
3. Imaging of the abdomen by ultrasonography or
computed tomography (CT).
4. Echocardiography.
5. Positron emission tomography (PET) scans may aid
diagnosis of vasculitis or help selection of biopsy
sites.
6. Biopsy.

13. • Management:
• Continuous observation & examination.
• Give empirical therapy regimen in severe ill or
deteriorating patient.
• Regimen include:
• Aminoglycoside with ceftizidine (anti- pseudomonas
antibiotic).
• Vancomycin if IV catheter.
• Empirical use of glucocorticoids should avoided.

14. Fever in the injection drug-user:
• Infective organisms are introduced by non-sterile (often
shared) injection equipment.
• The risks increase with prolonged drug use and injection
into large veins of the groin and neck necessitated by
progressive thrombosis of superficial peripheral veins.
• The most common causes of fever are soft tissue or
respiratory infections.
• Clinical assessment:
A) Site of injection:
1- Femoral vein injection = deep venous thrombosis, false
aneurysm, compartment syndrome, ilio-psoas abscess, and
septic arthritis of the hip joint or sacroiliac joint.
2- Jugular vein injection = cerebrovascular complications.

15. 3- Subcutaneous and intramuscular injection = infection by
clostridial species, Tetanus, wound botulism, anthrax and gas
gangrene.
B) Technical details of injection:
• Sharing of needles and paraphernalia (including spoons and
filters) = blood-borne virus infection (e.g. HIV-1, hepatitis B or C
virus), mouth organisms (e.g. anaerobic streptococci,
Fusobacterium spp. and Prevotella spp.) and blood-stream
infection with Candida spp.
C) Substances injected:
• Injection of cocaine = vascular complications.
• Heroin = wound botulism with black tar heroin.
• Blood-borne virus status:
• HIV-1 and hepatitis virus tests or vaccinations for hepatitis
viruses should be recorded.
• Surreptitious use of antimicrobials:
• Addicts may use antimicrobials to self-treat infections, masking
initial blood culture results.

17. • Investigations:
1. Echocardiography - to detect infective endocarditis,
thromboembolic phenomena; or a new or previously
undocumented murmur “Staphylococcus aureusor other
organisms”.
2. Chest x ray - lung abscesses or pneumatoceles.
3. Aspiration - Any pathological fluid collections should be
sampled.
4. Urinary toxicology tests – a non-infectious cause.
5. Blood test – hepatitis B and C virus and HIV-1.
• Management:
• Empirical therapy:
a) Flucloxacillin or, if meticillin-resistant Staph. aureus give
glycopeptide (e.g. vancomycin) or lipopeptide
(e.g.daptomycin).
b) For localised infections of the skin and soft tissues give
oral flucloxacillin plus co-amoxiclav or clindamycin.

18. Other Causes of FEVER:
• Fever in the immunocompromised host:
• Those with congenital immunodeficiency, HIV infection, and
iatrogenic immunosuppression induced by: chemotherapy,
transplantation or immunosuppressant medicines.
• Neutropenic fever:
• A neutrophil count of less than 0.5 × 109/L and a single axillary
temperature above 38.5°C. Patients with neutropenia are
particularly prone to bacterial and fungal infection.
• Post-transplantation fever:
• Due to infection, episodes of graft rejection in solid organ
transplant recipients, or graft-versus-host disease.
• Those in the first month are mostly related to the underlying
condition or surgical complications.
• Those occurring 1–6 months after transplantation are
characteristic of impaired T-cell function.

19. Blood-stream infection (BSI):
• Blood-stream infection (BSI) is a frequent presentation of
infection.
• Also known as Positive blood culture.
• This can be community-acquired or hospital-acquired.
• BSI has an associated mortality of 15–40%, depending on
the setting, host and microbial factors.

20. • Clinical assessment:
• Host factors predisposing to infection include:
1. Skin disease, diabetes mellitus, injection drug use,
the presence of a central venous, urinary or
haemodialysis catheter.
2. Surgical procedures, especially those involving the
implantation of prosthetic materials.
• Physical examination should focus on:
• Signs of endocarditis. evidence of bone or joint
infection (tenderness or restriction of movement),
and abdominal or flank tenderness.
• Investigation:
• Avoid contamination “Isolation”.
• Blood culture, chest X-ray, urine culture, ultrasound,
other imaging of the abdomen, and Echocardiography.

21. • Treatment:
• Antimicrobial therapy and surgical drainage if
appropriate.
1. Two weeks of therapy – in Staph. aureus BSI from
“ central and peripheral venous catheter infections,
uncomplicated skin and soft tissue infections, and
for uncomplicated right-sided infective
endocarditis.
2. 4–6 weeks of therapy – in Other Staph. aureus
BSIs.

22. Sepsis:
• Signs and symptoms of a systemic inflammatory
response syndrome (SIRS) to a localized primary site
of infection.
• Viral, bacterial (60% gram -, 40% gram +), fungal and
parasitic disease.
• In previously health individual the source of infection
are “intra-abdominal, UTI, pneumonia”.
• Predisposing factors:
• DM, burn, neutropenia, liver cirrhosis,
lymphoproliferative disease, intravenous drug users,
vascular catheterazation, presence of indwelling
mechanical devices.

23. • Pathophysiology:
• The septic shock result from “microbial signals,
toxin, or body response by formation of (cytokines,
Prostaglandins, complement C5 system)”.
• Clinical feature:
1. Fever, Chills or
Hypothermia.
2. Hypotension & Oliguria.
3. Hyperventilation.
4. Change mental status.
5. Skin manifestation.
6. Focal sign of localized
site of infection.

25. • Investigation:
1. CBC = leukocytosis, thrombocytopenia, Hb.
2. Blood Culture = 20% - 40% positive.
3. Gram staining & culture media = if blood culture is negative.
4. Radiology:
5. Chest x-ray = normal, or pneumonia, or diffuse infiltration of
ARDS.
6. Ultrasound = abdominal or pelvic infection.
7. Urea, creatinine, electrolyte = if renal damage.
8. Liver function tests (LFTs) = raised bilirubin & Alkaline
phosphate, high level of aminotransferases (ATL, STL).
9. Urine & Sputum analyzes and culture.
10. Gram stain & culture of available for pus and body fluid.
11. Arterial blood gases and Blood glucose.
12. Coagulation profile = low serum fibrin, prolonged PT, presence
of D-dimer and elevated fibrin degradation products (FDP).

26. • Management:

27. Acute diarrhoea and vomiting:
• Acute diarrhoea, sometimes with vomiting, is the
predominant symptom in infective
gastroenteritis.
• Acute diarrhoea may also be a symptom of other
infectious and non-infectious diseases. Stress,
whether psychological or physical, can also
produce loose stools.
• Route of entrance through faecal–oral.
• Mechanism of transmission:
• Fomites, on contaminated hands, or in food or
water.

29. • Clinical assessment:
A) The history:
• Foods ingested, duration and frequency of diarrhoea,
presence of blood or steatorrhoea, abdominal pain and
tenesmus, and whether other people have been affected.
• Fever and bloody diarrhoea suggest an invasive, colitic,
dysenteric process.
• An incubation period of less than 18 hours = diarrhoea
caused by toxin-mediated food poisoning.
• An incubation period of longer than 5 days = diarrhoea
caused by protozoa or helminths.
• Shigellosis or cholera spread from Person-to-person spread.
B) Examination includes:
• Assessment of the degree of dehydration.
• Assessment for early signs of hypotension:
• Thirst, headache, altered skin turgor, dry mucous
membranes and postural hypotension.

31. • Investigations:
• Stool:
1. Inspection for blood.
2. Microscopy for leucocytes, ova, cysts and parasites.
3. Culture and detection of C. difficile toxin sought.
• Blood:
1. FBC and serum electrolytes = degree of inflammation and
dehydration.
2. Blood film for malaria parasites.
3. Blood clture
4. Urine cultures
• Chest X-ray if other than gastroenteritis.
• Management:
• Isolation to all patients with acute, potentially infective
diarrhoea to minimise person-to-person spread of infection.
• If the history suggests a food-borne source - public health
measures.

32. 1- Fluid replacement:
• Normal daily fluid intake in an adult is only 1–2 L.
• Oral rehydration solutions (ORS) therefore contain sugars, as
well as water and electrolytes.
• The volume of fluid replacement required should be estimated
based on the following considerations:
1- Replacement of established deficit:
• First 2–4 hours of presentation give replacement of 1–1.5 L,
either orally (ORS) or by intravenous infusion (normal saline).
2- Replacement of ongoing losses:
• Stool losses should be carefully charted,
• Give commercially 200 mL of ORS; one sachet per diarrhoea.
3- Replacement of normal daily requirement:
• Daily requirement of 1–1.5 L of fluid.
• This will be increased substantially in fever or a hot environment

33. 2- Antimicrobial agents:
• In non-specific gastroenteritis, routine use of antimicrobials
does not improve outcome and may lead to antimicrobial
resistance or side-effects.
• In EHEC (enterohaemorrhagic Escherichia coli) infections, the
use of antibiotics may make the complication of haemolytic
uraemic syndrome.
• Antibiotics are indicated in Shigella dysenteriae, invasive
salmonellosis, & cholera epidemics.
3- Antidiarrhoeal, antimotility and antisecretory agents:
• These agents are not usually recommended in acute infective
diarrhoea.
• Loperamide, diphenoxylate and opiates are potentially
dangerous in dysentery in childhood, causing intussusception.
• Antisecretory agents, such as bismuth and chlorpromazine, may
make the stools appear more bulky but do not reduce stool fluid
losses and may cause significant sedation.
• Adsorbents, such as kaolin or charcoal, have little effect.