Travel conditions Flashcards
Tests used in HIV diagnosis
A) Antibody test: antibodies against HIV
B) Antibody/antigen test: antibodies against HIV and HIV antigen (virus itself)
C) RNA/DNA test: screen for viral RNA -> detects virus directly & DNA -> copies of viral
RNA
• Antibody/antigen test is recommended for screening purposes -> better for identifying
early infection
• The other tests are recommended as confirmatory tests (as follow up after positive result
of antibody/antigen test)
HIV diagnostic workout
Aims of HIV management with anti-retroviral therapy
What tests are involved in Dx of Malaria?
Why it’s important to know % of RBCs infected by parasite? (in malaria)
% of RBCs infected by parasites is
important -> patients with >5% parasitemia can have worse outcome
Common lab findings in malaria
Common lab findings:
- thrombocytopenia -> low platelet count
- elevated lactate levels -> due to hemolysis
- anaemia: normochromic (normal colour) and normocytic (normal size) BUT anaemia = low RBCs number
Management algorithm in ‘suspected’ malaria case
Types of malaria treatment (4)
- Suppressive treatment = Chemoprophylaxis is aimed to kill sporozoites before they infect hepatocytes -> given to travellers that go to endemic malaria countries
• Therapeutic treatment: to eliminate merozoites that are in erythrocytic phase -> given during active infection
- Gametocidal treatment - to kill gametocytes -> prevent spread of diseases
• Radical treatment - to kill hypnozoites in the liver (P. Vivax and P . Ovale infections)
Name (2) agents used to treat malaria
chloroquine, quinine
(2) options for malaria prevention - environmental
- to prevent mosquitoes from biting -> sprays, full body clothing, sleeping in the nets
- to remove containers with water -> as mosquitoes like to lay their eggs there (to control
mosquitoes population)
What virus family causes Viral Haemorrhagic Fever?
Flaviviridae virus family
What is the danger of viral haemorrhagic fever?
They can cause fever and bleeding disorders -> possible progression into shock and deaths
Pathogenesis of viral haemorrhagic fever
Symptoms of viral haemorrhagic fever
What are general blood test findings in a person with viral hemorrhagic fever?
- decrease in total WBC (particularly in the lymphocytes)
- decrease in platelet count
- increase in blood serum liver enzymes
- reduced clotting ability -> measured as increased PT and PTT times
- hematocrit may be elevated
- urea and creatinine may be raised (depends on hydration status of the patient)
- prolonged bleeding time
What is hematocrit?
*hematocrit - volume in % of RBCs; normally is around 47% (+/-5%) for men & 42% (+/- 5%) for women)
management of viral hemorrhagic fever
- may require intensive support care
- antiviral therapy -> IV ribavirin (useful in some cases of VHF)
Why do deaths usually occur in Ebola?
death occurs usually from low BP from fluid loss
- usually 6-16 days after the symptoms appear
- 50% of infected people die
Simple pathology of Ebola
- Ebola virus enters the immune cells -> infects it -> inflammatory molecules are secreted from an infected cell -> inflammatory process starts; also virus replicated within the cell (as per normal viral mechanism -> hijacking the cell to make new viruses)
- inflammatory molecules -> damage to vascular integrity -> hemorrhagic fever
Signs and symptoms of Ebola
Start usually 2 days - 3 weeks after contracting the virus
A. Early: fever, headache, muscle pain, sore throat (initially remains of a flu-like illness)
B. Later: vomiting, diarrhoea, rash and decreased renal and liver function *
* at later stage -> possible internal and external bleeding
Complications of Ebola
- progression into disseminated intravascular coagulation (DIC) -> presents as low platelet count and elevated D-dimer
- diffuse /rozproszony/ haemorrhage -> shock
- multi-organ dysfunction
- renal and hepatic dysfunction -> elevated creatinie and liver enzymes
How to make a diagnosis of Ebola from the results?
A. History, S&S
B. Decreased WBC -> then elevated WBC
C. D-Dimer -> elevated
D. platelet count decreased (DIC)
E. Prolonged PT and PTT (due DIC)
F. Liver enzymes -> elevated (hepatic dysfunction)
G. Urea and creatinine -> elevated (renal dysfunction)
E.ELISA (antigen recognition test) and PCR
IgM and IgG detection in Ebola (timeframes)
- IgM detected 2 days after symptom onset
- IgG antibodies 6- 18 days after symptom onset
Management of a patient with Ebola
* prevention measures (washes,disinfection, contact tracing, isolation, protective equipment, safe disposal, safe burial etc.)
- Supportive care as no specific treatments are available
- No licensed vaccine or anti-Ebola products developed
Supportive:
- Rehydration via oral or IV route
- analgesia
- nausea, fever and anxiety treatments
- blood products (fresh frozen plasma, RBCs, platelets)
- Heparin -> in effort to prevent DIC
- Clotting factors -> to decrease haemorrhage
Intensive care in developed worlds: maintaining blood volume and electrolytes (salt) balance, treating any bacterial infections that may develop
What meds and why to avoid in Ebola
*avoid ibuprofen or aspirin -> as risk of bleeding
How to distinguish Dengue from Ebola?
They are both types of viral haemorrhagic fever
distinction from Ebola: no renal/hepatic failure, no DIC
WHat virus causes Dengue?
mosquito-borne, tropical disease -> caused by dengue virus (enveloped, single stranded, positive sense, RNA virus)
Symptoms of Dengue infection
*start 3 - 14 days after infection
High fever, headache, vomiting, muscle and joint pain, characteristic skin rash
What’s prognosis in Dengue?
- Recovery usually takes <2 - 7 days
- Complication (in small proportion of cases), potentially fatal:
A. Dengue hemorrhagic fever -> bleeding, low platelet count, blood plasma leakage
B. Dengue shock -> extremely low BP
Diagnosis of Dengue
Diagnosis made on basis of S&S and physical examination -> however early manifestationsare difficult to be differentiated from other viral diseases/infections
Number of different tests available for diagnosis:
- detection of antibodies to the virus
- detection of viral RNA
Management of Dengue
No specific anti-viral drug is available
Rx depends on a status of a person:
- those whose hydration status is OK (drinking and passing urine) and are otherwise healthy (no warning signs) -> can be managed at home with daily follow-up and oral rehydration therapy
- patients with hydration and other health problems -> need to be hospitalised for a regular follow up
A. Preventative: vaccine available, reduction mosquito habitat, limitation of exposure to bites
B. Acute dengue fever -> supportive treatment:
- fluids (oral or IV) - mild to moderate disease
- blood transfusion - for severe forms of disease (if haematocrit is decreasing and vital signs are unstable)
What to avoid in pt with Dengue?
To avoid:
- invasive medical procedures e.g. NG tube, IM injections etc -> as risk of bleeding
- Do not use NSAIDs as they may increase risk of bleeding
*use Paracetamol (acetaminophren) instead (for fever and pain relief)
What’s atypical pneumonia?
Atypical pneumonia aka walking pneumonia
- pneumonia that is not caused by one of commonly pneumonia causing organisms
- different clinical presentation to that of a typical pneumonia
Difference between typical vs atypical pneumonia
- antibiotics used to Rx
- appearance on X ray
Difference between typical vs atypical pneumonia
- clinical presentation
Cause of Ameobic Abscess
- liver abscess caused by amebiasis -> as liver tissue is involved in the infection by thropozoites of Entamoeb histolytica -> abscess due to necrosis
Symptoms and signs of amoebic abscess
Symptoms:
- pain in R hypochondriac area (referred to R shoulder)
- pyrexia
- sweating and rigors
- loss of weight
- earthy complexion - patchy pigmentation of the face
Signs:
- pallor
- tenderness in R hypochondriac area
- palpable liver
- intercostal tenderness
- basal lung signs
Management of amoebic abscess
A.Abscess aspiration
B.Repeated liver imaging
C.Metronidazole - antibiotic and antiprotozoal medication
What is the cause of Leptospirosis?
- how is it spread
- who is at risk
Caused by a bacteria called Leptospira
- spread by wild and domestic animals (rodents e.g. rats, mice, hamsters, squirrels)
*in developing world - farmers and low-income people living in the cities and slums
* in the developed world - outdoor activities in warm and wet areas
Signs and symptoms of leptospirosis
S&S may range from:
A) none to mild: headaches, muscle pains, fevers
B) severe: bleeding from the lungs or meningitis
(2) serious complications of Leptospirosis
- Weil’s disease -> when a person infected with leptospira turns yellow, have kidney failure and bleeding (death rate >10%)
- Severe pulmonary haemorrhage syndrome -> bleeding into the lungs (death rate >50%)
Diagnosis/Ix of Leptospirosis
Early diagnosis - test blood and urine:
- blood and CSF -> infection can be found within first 10 days
- after 10 days -> infection moves to kidney -> can be found in fresh urine
- U&Es and LFTs, creatinine and nitrogen
- enzyme- linked immunosorbent assay (ELISA) and PCR -> confirm diagnosis
- MAT (microscopic agglutination test) -> gold standard in diagnosis of leptospirosis
Occupations at risk of Leptospirosis
Occupations at risk: vets, slaughterhouse workers, farmers, sailors, waste disposal
workers
Adventure tourism: kayakers, rowers, canoeists
Treatment of Leptospirosis
A. Usually effective antibiotics - Penicillin G, ampicillin, amoxicillin, deoxycline
B. More severe cases: cefotaxime or ceftriaxone
C. Glucose and salt infusions
D. Dialysis - if kidney affected severly
E. Measure potassium (as elevation is common)
Cause of Schistosomiasis
Schistosomiasis aka ‘snail fever’
- disease caused by parasitc flatworms (schistosomes)
- Parasites infect fresh water snails
Schistosomiasis
- site of infection
- long- term complications
- Sites of infection: urinary tract or intestine
- long time infection may result in: liver damage, kidney failure, bladder cancer, infertility
Risk groups of schistosomiasis
- Disease is particularly common among children in developing countries -> as they play a lot in fresh water (water is contaminated with shistosomes)
- farmers, fishermen, people using unclean water
Symptoms of schistosomiasis
Symptoms: abdominal pain, diarrhoea, bloody stool, blood in the urine
Children: poor growth and learning difficulties
Dx / Ix of schistosomiasis
- finding eggs of the parasite in a person’s urine or stool
- finding antibodies against the disease in the blood
Prevention of Schistosomiasis
- improving access to clean water
- reduction of water snail population
- meds Praziquantel (drug against some parasites) given once yearly to the populations at risk
Treatment of Schistosomiasis
All cases of schistosomiasis should be treated regardless of presentation -> as parasite can live in host for years
Preferably use Praziquantel (drug against some parasites) and combination of other
drugs (mostly these used to treat malaria as anti-parasitic activity)
Exotoxin mechanism of diarrhoea + bacteria causing it
- exotoxins -> effect on the stomach, small bowel -> mucosal inflammation symptoms of food poisoning (Bacillus Cereus and Staphylococus Aureus)
Enterotoxin mechanism of diarrhoea + bacteria causing it
enterotoxins -> watery diarrhoea without fever (E. Coli) - usually no blood or mucous
Enteroinvasive mechanism of diarrhoea + bacteria causing it
enteroinvasive -> invade intestinal mucosa (Enteroinvasive E. Coli, Shigella and Campylobacter) -> fewer, lower abdominal pain, bleeding diarrhoea + fever (dysentery)
Possible complications of diarrhoea
electrolyte imbalances, renal impairment, dehydration, defective immune responses, inefficiency of administrated drug -> as medication travels too quickly through digestive tract
Medical management of diarrhoea
- Oral rehydration therapy -> slightly sweetened and salty water -> used to prevent dehydration; it can be given via NG tube; usually include zinc
supplementation
- Medication: antibiotics used only in certain cases of diarrhoea (bacterial) - > beneficial in resource poor countries; antibiotics may contribute to diarrhoea
Other medications (used only if the bloody diarrhoea is not present):
- Bismuth compounds (Pepto-Bismol) -> decreases number of bowel movements in traveler’s diarrhoea but do not decrease length of illness
- Loperamide -> anti motility agent -> to reduce number of stools but again, not the illness duration
- Bile acid sequestrants (bile reabsorption prevented from the gut) -> for those with chronic diarrhoea due to bile acid malabsorption
- Zinc supplementation -> beneficial for children over 6 months old
- Probiotics -> reduce duration of symptoms by one day + reduce chance of symptoms lasting longer than 4 days (by 60%)
Diet recommendation in diarrhoea
- Fluid and food: Replacing lost fluids (usually by oral rehydration therapy), in severe cases IV
- diet restrictions are not recommended (even for babies and children; including those breast fed) -> as nutrient is usually still absorbed and support children with growth and also eating as usual has an effect on speed up of recovery as support normal intestinal functioning; limitation of food has no effect on duration of diarrhoea
Antibiotic-associated diarrhoea
- common bacteria
- severe form (names )
- age groups at risk
- when develops
- bacterial overgrowth with C. Difficile
- severe -> can lead to acute colitis/ pseudomembranous colitis
- common in young and elderly
- diarrhoea develops 2 days - 4 weeks after taking antibiotics
Risk factors for C Diff infection
Risk factors: Prolonged hospital stay, multiple or prolonged antibiotic therapy, GI surgery, proton pump inhibitor use
Ix and what can be seen in C Diff
- detection of C.Diff toxins (in stool by enzyme-linked immunosorbent assay ELISA)
- stool culture -> C diff isolation (in 30%)
- sigmoidoscopy -> ulceration and a white pseudomembrane
Management of C Diff infection
- antibiotics should be stopped
- to treat dehydration (oral, IV fluids)
- infection control measures) -> barrier nursing and hand washing
- antibiotics against C.Diff (metronizadole or oral vancomycin) should be started following a diagnosis
- more severe in the elderly -> colectomy may be required for toxic megacolon
