Infectious disease 2 Flashcards
PRimary TB symptoms?
Asymptomatic primary infection
primary infection with TB may be asymptomatic
Symptomatic primary infection
fever
pleuritic or retrosternal pain
pleuritic pain may be secondary to a pleural effusion
retrosternal pain may be secondary to enlarged bronchial lymph nodes
Secondary TB symptoms?
cough
gradually becoming productive
haemoptysis is only seen in a minority
weight loss
fatigue
night sweats
fever: typically low-grade
Complications of TB?
Tuberculous adrenalitis is a well-described complication, usually resulting from the haematogenous spread of bacilli from other sites. Untreated, it causes progressive destruction of the adrenal glands leading to hypoadrenalism.
Pulmonary tuberculosis: Persistent coughing, chest pain, and haemoptysis are common symptoms. Complications include bronchiectasis, chronic obstructive pulmonary disease (COPD), lung abscesses, and pneumothorax.
Miliary tuberculosis: This disseminated form can affect multiple organs including the liver, spleen, bone marrow and meninges causing hepatosplenomegaly, pancytopenia or meningitis respectively.
Tuberculous meningitis: A severe form of TB that predominantly affects children. Symptoms may include headache, fever, vomiting and altered mental status. It may lead to hydrocephalus or brain infarcts due to inflammation of cerebral vasculature.
Skeletal tuberculosis: Also known as Pott’s disease when it involves the spine. It can cause vertebral collapse leading to kyphosis or paraplegia due to spinal cord compression.
Genitourinary tuberculosis: Can result in renal impairment or infertility.
Gastrointestinal tuberculosis: May present with abdominal pain and bowel obstruction secondary to strictures.
What should be given in a pre-hospital setting if meningitis suspected?
IM ben pen
as long as it does not delay transfer
What are warning signs of bacterial meningitis?
rapidly progressive rash
poor peripheral perfusion
respiratory rate < 8 or > 30 / min or pulse rate < 40 or > 140 / min
pH < 7.3 or WBC< 4 *109/L or lactate > 4 mmol/L
GCS < 12 or a drop of 2 points
poor response to fluid resuscitation
When should LP be delayed in suspected bacterial meningitis?
signs of severe sepsis or a rapidly evolving rash
severe respiratory/cardiac compromise
significant bleeding risk
signs of raised intracranial pressure
focal neurological signs
papilloedema
continuous or uncontrolled seizures
GCS ≤ 12
Managament of bacteral meningitis?
LP (if this can not be done within the first hour - abx should be given after blood cultureshave been taken)
IV antibiotics
3 months - 50 years: BNF recommends cefotaxime (or ceftriaxone)
> 50 years: BNF recommends cefotaxime (or ceftriaxone) + amoxicillin (or ampicillin) for adults
When should IV dexamethasone be given in suspected bacterial meningnits?
the BNF recommend to ‘consider adjunctive treatment with dexamethasone (particularly if pneumococcal meningitis suspected in adults), preferably starting before or with first dose of antibacterial, but no later than 12 hours after starting antibacterial; avoid dexamethasone in septic shock, meningococcal septicaemia, or if immunocompromised, or in meningitis following surgery’
How to manage patients with suspected bacterial meningitis and signs of raised ICP?
get critical care input
secure airway + high-flow oxygen
IV access → take bloods and blood cultures
IV dexamethasone
IV antibiotics as above
arrange neuroimaging
What should CSF be tested for in suspected meningitis?
glucose, protein, microscopy and culture
lactate
meningococcal and pneumococcal PCR
enteroviral, herpes simplex and varicella-zoster PCR
consider investigations for TB meningitis
what type of virus is hep c?
RNA flavivirus
What is the incubation period of hep c?
6-9 weeks
How is hep c transmitted?
the risk of transmission during a needle stick injury is about 2%
the vertical transmission rate from mother to child is about 6%. The risk is higher if there is coexistent HIV
breastfeeding is not contraindicated in mothers with hepatitis C
the risk of transmitting the virus during sexual intercourse is probably less than 5%
there is no vaccine for hepatitis C
Symptoms of hep c?
After exposure to the hepatitis C virus only around 30% of patients will develop features such as:
a transient rise in serum aminotransferases / jaundice
fatigue
arthralgia
Investigations for Hep c?
HCV RNA is the investigation of choice to diagnose acute infection
whilst patients will eventually develop anti-HCV antibodies it should be remembered that patients who spontaneously clear the virus will continue to have anti-HCV antibodies
How many patient who have hep c develop chronic infection?
around 15-45% of patients will clear the virus after an acute infection (depending on their age and underlying health) and hence the majority (55-85%) will develop chronic hepatitis C
what is chronic hep c defined as ?
Chronic hepatitis C may be defined as the persistence of HCV RNA in the blood for 6 months.
Complications of hep c ?
rheumatological problems: arthralgia, arthritis
eye problems: Sjogren’s syndrome
cirrhosis (5-20% of those with chronic disease)
hepatocellular cancer
cryoglobulinaemia: typically type II (mixed monoclonal and polyclonal)
porphyria cutanea tarda (PCT): it is increasingly recognised that PCT may develop in patients with hepatitis C, especially if there are other factors such as alcohol abuse
membranoproliferative glomerulonephritis
management of chronic hep c?
reatment depends on the viral genotype - this should be tested prior to treatment
the management of hepatitis C has advanced rapidly in recent years resulting in clearance rates of around 95%. Interferon based treatments are no longer recommended
the aim of treatment is sustained virological response (SVR), defined as undetectable serum HCV RNA six months after the end of therapy
currently a combination of protease inhibitors (e.g. daclatasvir + sofosbuvir or sofosbuvir + simeprevir) with or without ribavirin are used
What does clostridium tetani lead to?
It is a neurotoxin (tetanospasmin)
Blocks the release of the inhibitory neurotransmitters GABA and glycine resulting in continuous motor neuron activity → continuous muscle contraction → lockjaw and respiratory paralysis
what are exotoxins and endotoxins?
Exotoxins are secreted by bacteria where as endotoxins are only released following lysis of the cell. Exotoxins are generally released by Gram positive bacteria with the notable exceptions of Vibrio cholerae and some strains of E. coli
Endotoxins are lipopolysaccharides that are released from Gram-negative bacteria such as Neisseria meningitidis.
How are extoxins classified
pyrogenic toxins
enterotoxins
neurotoxins
tissue invasive toxins
miscellaneous toxins
what are pyrogenic toxins?
Pyrogenic toxins stimulate the release of endogenous cytokines resulting in fever, rash etc. They are superantigens which bridge the MHC class II protein on antigen-presenting cells with the T cell receptor on the surface of T cells resulting in massive cytokine release.
What are examples of pyrogenic toxins
what are enterotoxins?
Enterotoxins act on the gastrointestinal tract causing one of two patterns of illness:
diarrhoeal illness
vomiting illness (‘food poisoning’)
Examples of enterotoxins?
what are neurotoxins?
Neurotoxins act on the nerves (tetanus) or the neuromuscular junction (botulism) causing paralysis.
Examples of neurotoxins?
Examples of tissue invesive toxins?
What does the diptheria toxin lead to ?
ADP ribosylates elogation factor (EF-2), resulting in inhibition, causing a ‘diphtheric membrane’ on tonsils caused by necrotic mucosal cells. Systemic distribution may produce necrosis of myocardial, neural and renal tissue
What factors will reduce the vertical transmission of HIV?
Factors which reduce vertical transmission (from 25-30% to 2%)
maternal antiretroviral therapy
mode of delivery (caesarean section)
neonatal antiretroviral therapy
infant feeding (bottle feeding)
mode of delivery in HIV +ve patients?
vaginal delivery is recommended if viral load is less than 50 copies/ml at 36 weeks, otherwise caesarian section is recommended
a zidovudine infusion should be started four hours before beginning the caesarean section
Neonatal antiretroviral therapy?
zidovudine is usually administered orally to the neonate if maternal viral load is <50 copies/ml. Otherwise triple ART should be used. Therapy should be continued for 4-6 weeks.
Breast feeding iin HIV +ve mothers?
in the UK all women should be advised not to breast feed
Anti-malarials used and their side effects?
Anti-malarials in pregnancy?
chloroquine can be taken
proguanil: folate supplementation (5mg od) should be given
Malarone (atovaquone + proguanil): the BNF advises to avoid these drugs unless essential. If taken then folate supplementation should be given
mefloquine: caution advised
doxycycline is contraindicated
Causes of gastroenteritis?
The most common cause is E.coli
Giardiasis
Cholera
Shigella
S.aureus
campylobacter
Bacillus cereus
Amobiasis
Incubation period
1-6 hrs: Staphylococcus aureus, Bacillus cereus*
12-48 hrs: Salmonella, Escherichia coli
48-72 hrs: Shigella, Campylobacter
> 7 days: Giardiasis, Amoebiasis
Meningitis CSF analysis for bacterial, viral, TB and fungal?
Basic facts about staphylococci?
Gram-positive cocci
facultative anaerobes
produce catalase
What are the two main types of Staphylococcus?
S.Aureus
* Coagulase-positive
* Causes skin infections (e.g. cellulitis), abscesses, osteomyelitis, toxic shock syndrome
S.epidermidis
* Coagulase-negative
* Cause of central line infections and infective endocarditis
what are Rickettsiae?
Rickettsiae are Gram-negative obligate intracellular parasites. Types of rickettsiae cause a variety of diseases that are typically characterised by fever, headache and rash. A notable exception is Q fever (cause by Coxiella burnetti which causes pneumonia but no rash. The Weil-Felix reaction is positive except in Q fever. Rickettsial diseases are all treated with tetracyclines.
What causes rocky mountain spotted fever?
Rickettsia ricketsii
Ticks carru the disease
Headache and fever are common
Rash starts on the peripheries (wrist, ankles) before spreading centrally. It is initially maculopapular before becoming vasculitic
Endemic to east coast of US
What causes Q fever?
Coxiella burnetti
No rash but causes pneumonia
what causes endemic typhus?
Rickettsia typhi -Carried by Flaes
Rash starts centrally then spreads to the peripheries
What causes epidemic typhus?
Rickettsia prowazekii - caused by human body louce
what causes diptheria?
Diphtheria is caused by the Gram positive bacterium Corynebacterium diphtheriae
Pathophysiology
releases an exotoxin encoded by a β-prophage
exotoxin inhibits protein synthesis by catalyzing ADP-ribosylation of elongation factor EF-2
Diphtheria toxin commonly causes a ‘diphtheric membrane’ on tonsils caused by necrotic mucosal cells. Systemic distribution may produce necrosis of myocardial, neural and renal tissue
Possible presentations of diptheria?
Possible presentations
recent visitors to Eastern Europe/Russia/Asia
sore throat with a ‘diphtheric membrane’ - grey, pseudomembrane on the posterior pharyngeal wall
bulky cervical lymphadenopathy
may result in a ‘bull neck’ appearanace
neuritis e.g. cranial nerves
heart block
Investigations for diptheria?
Investigations
culture of throat swab: uses tellurite agar or Loeffler’s media
Management for Diptheria?
intramuscular penicillin
diphtheria antitoxin
Identfiying gram positive bacteria?
Gram-positive bacteria will turn purple/blue following the gram staining. Microscopy will then reveal the shape, either cocci or rods.
Examples of gram positive rods?
Rods (bacilli)
Actinomyces
Bacillus antracis
Clostridium
Corynebacterium diphtheriae
Listeria monocytogenes
How to distiguish between gram positive cocci?
Cocci
makes catalase: Staphylococci
does not make catalase: Streptococci
Staphylococci
makes coagulase: S. aureus
does not make coagulase: S. epidermidis (novobiocin sensitive), S. saprophyticus (novobiocin resistant)
Streptococci
partial haemolysis (green colour on blood agar): α-haemolytic
complete haemolysis (clear): β-haemolytic
no haemolysis: γ-haemolytic
α-haemolytic streptococci
optochin sensitive: S. pneumoniae
optochin resistant: Viridans streptococci
β-haemolytic streptococci
bacitracin sensitive: Group A: S. pyogenes
bacitracin resistant: Group B: S. agalactiae
Causes of viral meningitis?
The most common causes of viral meningitis in adults are enteroviruses
non-polio enteroviruses e.g. coxsackie virus, echovirus
mumps
herpes simplex virus (HSV), cytomegalovirus (CMV), herpes zoster viruses
HIV
measles
Risk factors for viral meningitis?
patients at the extremes of age (< 5 years and the elderly)
immunocompromised, e.g. patients with renal failure, with diabetes
intravenous drug users
How does viral meningitis present?
common features
headache
evidence of neck stiffness
photophobia (often milder than the photophobia experienced by a patient with bacterial meningitis)
confusion
fevers
less common features
focal neurological deficits on examination
seizures: suggests a meningoencephalitis
Management of viral meningitis?
whilst awaiting the results of the lumbar puncture, treatment should be supportive and if there is any question of bacterial meningitis or of encephalitis, the patient should be commenced on broad-spectrum antibiotics with CNS penetration e.g. ceftriaxone and aciclovir intravenously. This is particularly the case if the patient has risk factors e.g. elderly, immunocompromised
generally speaking, viral meningitis is self-limiting, with symptoms improving over the course of 7 - 14 days and complications are rare in immunocompetent patients
aciclovir may be used if the patient is suspected of having meningitis secondary to HSV
what causes Kaposi’s sarcome?
caused by HHV-8 (human herpes virus 8)
how does Kaposi’s sarcoma present?
presents as purple papules or plaques on the skin or mucosa (e.g. gastrointestinal and respiratory tract)
skin lesions may later ulcerate
respiratory involvement may cause massive haemoptysis and pleural effusion
managment of kaposi’s sarcoma?
Radiotherapy and resection
What can cause a false positive non-treponemal (cardiolipin) test?
pregnancy
SLE, anti-phospholipid syndrome
tuberculosis
leprosy
malaria
HIV
Post exposure prophylaxsis for Hep A
Human Normal Immunoglobulin (HNIG) or hepatitis A vaccine may be used depending on the clinical situation
Post exposure prophylaxsis for hep B?
HBsAg positive source
if the person exposed is a known responder to the HBV vaccine then a booster dose should be given
if they are a non-responder (anti-HBs < 10mIU/ml 1-2 months post-immunisation) they need to have hepatitis B immune globulin (HBIG) and a booster vaccine
unknown source
for known responders the HBV vaccine the Green Book advises considering a booster dose of HBV vaccine
for known non-responders HBIG + vaccine should be given whilst those in the process of being vaccinated should have an accelerated course of HBV vaccine
Post exposure prophylaxsis for hep c ?
monthly PCR - if seroconversion then interferon +/- ribavirin
Post exposure prophylaxsis for HIV?
a combination of oral antiretrovirals (e.g. Tenofovir, emtricitabine, lopinavir and ritonavir) as soon as possible (i.e. Within 1-2 hours, but may be started up to 72 hours following exposure) for 4 weeks
serological testing at 12 weeks following completion of post-exposure prophylaxis
reduces risk of transmission by 80%
Post exposure prophylaxsis for varicella zoster?
VZIG for IgG negative pregnant women/immunosuppressed
Features of Legionella?
flu-like symptoms including fever (present in > 95% of patients)
dry cough
relative bradycardia
confusion
lymphopaenia
hyponatraemia
deranged liver function tests
pleural effusion: seen in around 30% of patients
Investigations in legionella?
diagnositic test of choice:urinary antigen
chest x-ray findings are non-specific but may include:
a mid-to-lower zone predominance of patchy consolidation
pleural effusions in around 30%
Management of Legionella?
treat with erythromycin/clarithromycin
who does klebsiella pneurmoniae typically effect?
It typically affects alcohol-dependent individuals and those with diabetes mellitus, presenting with red currant jelly sputum and upper lobe consolidation on chest radiographs.
How does mycoplasma pneumoniae usually present?
characterised by dry cough and flu-like symptoms, it predominantly affects younger patients. Further although it typically also causes consolidation that would appear bilaterally on a chest X-ray, it often involves only involves the lower zones. Some patients may also experience complications such as erythema multiforme, pericarditis or myocarditis, gastrointestinal symptoms, or bullous myringitis.
Aetiology of Dengue fever?
Dengue fever is a viral infection that can progress to viral haemorrhagic fever (other examples include yellow fever, Lassa fever, Ebola).
Aetiology
dengue virus is a RNA virus of the genus Flavivirus
transmitted by the Aedes aegypti mosquito
incubation period of 7 days
how may Dengue fever be classified?
dengue fever:
without warning signs
with warning signs
severe dengue (dengue haemorrhagic fever)
Symptoms of Dengue fever?
fever
headache (often retro-orbital)
myalgia, bone pain and arthralgia (‘break-bone fever’)
pleuritic pain
facial flushing (dengue)
maculopapular rash
haemorrhagic manifestations e.g. positive tourniquet test, petechiae, purpura/ecchymosis, epistaxis
‘warning signs’ include:
abdominal pain
hepatomegaly
persistent vomiting
clinical fluid accumulation (ascites, pleural effusion)
Symptoms of Severe dengue (dengue haemorrhagic fever)?
this is a form of disseminated intravascular coagulation (DIC) resulting in:
thrombocytopenia
spontaneous bleeding
around 20-30% of these patients go on to develop dengue shock syndrome (DSS)
How is Dengue fever diagnosed?
typically blood results
leukopenia, thrombocytopenia, raised aminotransferases
diagnostic tests
serology
nucleic acid amplification tests for viral RNA
NS1 antigen test
Treatment of Dengue fever?
entirely symptomatic e.g. fluid resuscitation, blood transfusion etc
no antivirals are currently available
What are the symptoms and treatment of Chikungunya?
Prominent symptoms are severe joint pain and abrupt onset of high fever. Other symptoms include general flu-like illness of muscle ache, headache, and fatigue. The disease shares its symptoms with dengue but tends to have more joint pain which can be debilitating. A rash may develop as with other viral illness and swelling of the joints in not uncommon.
Treatment: Relief of symptoms. No specific treatment.
Alphavirus disease caused by infected mosquitoes
Management of mycoplasma pneumoniae?
doxycycline or a macrolide (e.g. erythromycin/clarithromycin)
what organism is seen in animal bites?
The majority of bites seen in everyday practice involve dogs and cats. These are generally polymicrobial but the most common isolated organism is Pasteurella multocida.
Management of animal bites?
cleanse wound. Puncture wounds should not be sutured closed unless cosmesis is at risk
current BNF recommendation is co-amoxiclav
if penicillin-allergic then doxycycline + metronidazole is recommended
bacteria seenin human bites?
Human bites commonly cause multimicrobial infection, including both aerobic and anaerobic bacteria.
Common organisms include:
Streptococci spp.
Staphylococcus aureus
Eikenella
Fusobacterium
Prevotella
Co-amoxiclav is recommended, as for animal bites.
What is Parvovirus B19?
Parvovirus B19 is a DNA virus which causes a variety of clinical presentations. It was identified in the 1980’s as the cause of erythema infectiosum
Erythema infectiosum (also known as fifth disease or ‘slapped-cheek syndrome’)
The illness may consist of a mild feverish illness which is hardly noticeable. However, in others there is a noticeable rash which appears after a few days. The rose-red rash makes the cheeks appear bright red, hence the name ‘slapped cheek syndrome’. The rash may spread to the rest of the body but unlike many other rashes, it only rarely involves the palms and soles.
The child begins to feel better as the rash appears and the rash usually peaks after a week and then fades. The rash is unusual in that for some months afterwards, a warm bath, sunlight, heat or fever will trigger a recurrence of the bright red cheeks and the rash itself. Most children recover and need no specific treatment. School exclusion is unnecessary as the child is not infectious once the rash emerges. In adults, the virus may cause acute arthritis.
do children need to be excluded from school with erythema infectiosum?
(slapped cheek syndrome)
It is spread by the respiratory route and a person is infectious 3 to 5 days before the appearance of the rash. Children are no longer infectious once the rash appears and there is no specific treatment.
The child need not be excluded from school as they are no longer infectious by the time the rash occurs.
Other presentations of parvo virus b19?
asymptomatic
pancytopaenia in immunosuppressed patients
aplastic crises e.g. in sickle-cell disease
parvovirus B19 suppresses erythropoiesis for about a week so aplastic anaemia is rare unless there is a chronic haemolytic anaemia
hydrops fetalis
Parvovirus B19 in pregnant woman?
parvovirus B19 in pregnant women can cross the placenta in pregnant women
this causes severe anaemia due to viral suppression of fetal erythropoiesis → heart failure secondary to severe anaemia → the accumulation of fluid in fetal serous cavities (e.g. ascites, pleural and pericardial effusions)
**treated with intrauterine blood transfusions
**
features of tetanus?
prodrome fever, lethargy, headache
trismus (lockjaw)
risus sardonicus: facial spasms
opisthotonus (arched back, hyperextended neck)
spasms (e.g. dysphagia)
Management of tetanus?
Management
supportive therapy including ventilatory support and muscle relaxants
intramuscular human tetanus immunoglobulin for high-risk wounds (e.g. compound fractures, delayed surgical intervention, significant degree of devitalised tissue)
metronidazole is now preferred to benzylpenicillin as the antibiotic of choice
What should be considered in the presentation of dysenery after long incubation periosd?
Amoebiasis should be considered
The history of abdominal pain, gradual onset bloody diarrhoea, and a long incubation period in a returning traveller is highly suggestive of amoebiasis dysentery. The causative organism for amoebiasis is Entamoeba histolytica.
What kind of bacteria is E.coli?
Escherichia coli is a facultative anaerobic, lactose-fermenting, Gram negative rod which is a normal gut commensal.
what os E. coli O157:H7?
E. coli O157:H7 is a particular strain associated with severe, haemorrhagic, watery diarrhoea. It has a high mortality rate and can be complicated by haemolytic uraemic syndrome. It is often spread by contaminated ground beef.
what can E.coli cause?
diarrhoeal illnesses
UTIs
neonatal meningitis
What is the mininmal interval required between giving two live vaccinations?
Live vaccines given by injection may be either given concomitantly or a minimum interval of 4 weeks apart to prevent risk of immunological interference
To prevent the risk of immunological interference
What type of bacteria is Clostridia?
Clostridia are gram-positive, obligate anaerobic bacilli.
What does clostridia botulinum lead to?
typically seen in canned foods and honey
prevents acetylcholine (ACh) release leading to flaccid paralysis
What does clostdia perfringens lead to?
produces α-toxin, a lecithinase, which causes gas gangrene (myonecrosis) and haemolysis
features include tender, oedematous skin with haemorrhagic blebs and bullae. Crepitus may present on palpation
what does colstrdia tetani lead to?
produces an exotoxin (tetanospasmin) that prevents the release of glycine from Renshaw cells in the spinal cord causing a spastic paralysis
what causes fish tank granulonma?
Mycobacterium marinum is one of many mycobacteria that can cause disease in humans. Fish tank granuloma typically presents in patients who have had an exposure to, or frequently work with fish.
How does fish tank granuloma present?
It has an incubation period of 3-4 weeks and lesions can be painful or painless. A cut or break in the skin can be enough for the organism to enter the blood stream and track up the lymphatic system (sporotrichoid spread).
Treatent for fish tank granuloma?
Treatment options include tetracyclines, fluoroquinolones, sulfonamides and macrolides.
what is yellow fever and what causes it?
Type of viral haemorrhagic fever (also dengue fever, Lassa fever, Ebola).
Basics
zoonotic infection: spread by Aedes mosquitos
incubation period = 2 - 14 days
Features of yellow fever?
Features
may cause mild flu-like illness lasting less than one week
classic description involves sudden onset of high fever, rigors, nausea & vomiting. Bradycardia may develop. A brief remission is followed by jaundice, haematemesis, oliguria
if severe jaundice, haematemesis may occur
Councilman bodies (inclusion bodies) may be seen in the hepatocytes
What causes Lymphogranuloma venereum?
Lymphogranuloma venereum (LGV) is caused by Chlamydia trachomatis serovars L1, L2 and L3*.
Risk factors for lymphgranuloma venereum?
men who have sex with men
the majority of patients who present in developed countries have HIV
historically was seen more in the tropics
Symptoms of lymphgranuloma venereum
Typically infection comprises of three stages:
stage 1: small painless pustule which later forms an ulcer
stage 2: painful inguinal lymphadenopathy
may occasionally form fistulating buboes
stage 3: proctocolitis
Treatment of lymphgranuloma venereum?
Doxycycline
HIV seroconversion?
HIV seroconversion is symptomatic in 60-80% of patients and typically presents as a glandular fever-type illness. Increased symptomatic severity is associated with poorer long-term prognosis. It typically occurs 3-12 weeks after infection
Features
sore throat
lymphadenopathy
malaise, myalgia, arthralgia
diarrhoea
maculopapular rash
mouth ulcers
rarely meningoencephalitis
What are the most common causes of non-falcparum malaria?
Plasmodium vivax, with Plasmodium ovale and Plasmodium malariae accounting for the other cases. Plasmodium vivax is often found in Central America and the Indian Subcontinent whilst Plasmodium ovale typically comes from Africa.
Plasmodium knowlesi is another non-falciparum species which causes clinical pathology, found predominantly in South East Asia.
Features of non-falciparum malaria?
Features
general features of malaria: fever, headache, splenomegaly
Plasmodium vivax/ovale: cyclical fever every 48 hours. Plasmodium malariae: cyclical fever every 72 hours
Plasmodium malariae: is associated with nephrotic syndrome.
Ovale and vivax malaria have a hypnozoite stage and may therefore relapse following treatment.
Treatment of non-falciparum malaria?
in areas which are known to be chloroquine-sensitive then WHO recommend either an artemisinin-based combination therapy (ACT) or chloroquine
in areas which are known to be chloroquine-resistant an ACT should be used
ACTs should be avoided in pregnant women
patients with ovale or vivax malaria should be given primaquine following acute treatment with chloroquine to destroy liver hypnozoites and prevent relapse
What does Cryptosporidiosis causes?
Cryptosporidiosis is the commonest protozoal cause of diarrhoea in the UK. Two species, Cryptosporidium hominis and Cryptosporidium parvum account for the majority cases.
Cryptosporidiosis is more common in immunocompromised patients (e.g. HIV) and young children.
Features of cryptosporidosis?
watery diarrhoea
abdominal cramps
fever
in immunocompromised patients, the entire gastrointestinal tract may be affected resulting in complications such as sclerosing cholangitis and pancreatitis
Diagnosis of Cryptosporidiosis
stool: modified Ziehl-Neelsen stain (acid-fast stain) of the stool may reveal the characteristic red cysts of Cryptosporidium
Management of Cryptosporidiosis?
is largely supportive for immunocompetent patients
if the patient has HIV and is not on antiretroviral therapy then this should be started and often will be enough to resolve the infection
nitazoxanide may be used for immunocompromised patients
rifaximin is also sometimes used for immunocompromised patients/patients with severe disease
What are the main tests available for HIV?
HIV antibody - enzyme-linked immunosorbent assays (ELISAs) are often used for screening
HIB antibody and HIV antigen
p24 antigen can be detected as early as 2-3 weeks after exposure
the sensitivity of these fourth-generation tests approaches 100% for patients with chronic HIV infection
now the first-line test for HIV screening of asymptomatic individuals or patients with signs and symptoms of chronic infection
HIV RNA (qualitative or quantitative) - may be useful for diagnosis of neonatal HIV infection and screening blood donors
most people develop antibodies to HIV at 4-6 weeks but 99% do by 3 months
What is Schistosomiasis?
Schistosomiasis, or bilharzia, is a parasitic flatworm infection. The three main species of schistosome are S. mansoni, S. japonicum and S. haematobium.
How may acute infection with schistosomiasis present?
Acute manifestations may include:
swimmers’ itch
acute schistosomiasis syndrome (Katayama fever)
fever
urticaria/angioedema
arthralgia/myalgia
cough
diarrhoea
eosinophilia
What is Schistosoma haematobium?
These worms deposit egg clusters (pseudopapillomas) in the bladder, causing inflammation. The calcification seen on x-ray is actually calcification of the egg clusters, not the bladder itself.
Depending on the site of these pseudopapillomas in the bladder, they can cause an obstructive uropathy and kidney damage.
This typically presents as a ‘swimmer’s itch’ in patients who have recently returned from Africa.
What cancer is Schistosoma haematobium a risk factor for?
squamous cell bladder cancer.
Features of Schistosoma haematobium?
frequency
haematuria
bladder calcification
Investigations and management for Schistosoma haematobium
Investigation
for asymptomatic patients serum schistosome antibodies are generally preferred
for symptomatic patients the gold standard for diagnosis is urine or stool microscopy looking for eggs
Management
single oral dose of praziquantel
Schistosoma mansoni and Schistosoma japonicum
These worms mature in the liver and then travel through the portal system to inhabit the distal colon. Their presence in the portal system can lead to progressive hepatomegaly and splenomegaly due to portal vein congestion.
These species can also lead to complications of liver cirrhosis, variceal disease and cor pulmonale.
