Infectious Diseases Flashcards
Leprosy, caused by Mycobacterium leprae features Sensory loss and hypopigmented skin lesions. What are commonest sites of the skin lesions?
typically affecting the buttocks, face, and extensor surfaces of limbs
The organism grows best at 27-30°C; therefore, skin lesions tend to develop in the cooler areas of the body, with sparing of the groin, axilla, and scalp.
Pathophysiology of paucibacillary versus multibacillary leprosy pathophysiology:
Low degree of cell mediated immunity → lepromatous leprosy (‘multibacillary’)
High degree of cell mediated immunity → tuberculoid leprosy (‘paucibacillary’)
Pathophysiology (medscape)
Leprosy can manifest in different forms, depending on the host response to the organism.
Individuals who have a vigorous cellular immune response to M leprae have the tuberculoid form of the disease that usually involves the skin and peripheral nerves. The number of skin lesions is limited, and they tend to be dry and hypoesthetic. Nerve involvement is usually asymmetric. This form of the disease is also referred to as paucibacillary leprosy because of the low number of bacteria in the skin lesions (ie, < 5 skin lesions, with absence of organisms on smear). Results of skin tests with antigen from killed organisms are positive in these individuals.
Individuals with minimal cellular immune response have the lepromatous form of the disease, which is characterized by extensive skin involvement. Skin lesions are often described as infiltrated nodules and plaques, and nerve involvement tends to be symmetric in distribution. The organism grows best at 27-30°C; therefore, skin lesions tend to develop in the cooler areas of the body, with sparing of the groin, axilla, and scalp. This form of the disease is also referred to as multibacillary leprosy because of the large number of bacteria found in the lesions (ie, >6 lesions, with possible visualization of bacilli on smear).
1) Features of paucibacillary leprosy and
2) treatment
1) Low degree of cell mediated immunity → lepromatous leprosy (‘multibacillary’)
extensive skin involvement
symmetrical nerve involvement
2) rifampicin and dapsone for 6 months
1) Features of multibacillary leprosy and
2) treatment
1) High degree of cell mediated immunity → tuberculoid leprosy (‘paucibacillary’)
limited skin disease
asymmetric nerve involvement
2) triple therapy with rifampicin, dapsone and clofazimine for 12 months
Shigella infection is usually self-limiting and does not require antibiotic treatment antibiotics (e.g. ciprofloxacin) except for…….
1) people with severe disease,
2) immunocompromised
3) bloody diarrhoea
higella infection is usually self-limiting and does not require antibiotic treatment
antibiotics are indicated for people with severe disease, who are immunocompromised or with bloody diarrhoea. What is appropriate antibiotic?
Cirpofloxacin
Clinical features of Trypanosoma rhodesiense
Trypanosoma chancre - painless subcutaneous nodule at site of infection
intermittent fever
enlargement of posterior cervical lymph nodes
later: central nervous system involvement e.g. somnolence, headaches, mood changes, meningoencephalitis
Treatment of Trypanosoma rhodesiense
Management Trypanosoma rhodesiense
early disease: IV pentamidine or suramin
later disease or central nervous system involvement: IV melarsoprol
What is the vector for trypansoaoma Cruzi
Triatomine bugs
What is treatment for Trypanosoma Cruzi?
Management
treatment is most effective in the acute phase using azole or nitroderivatives such as benznidazole or nifurtimox
chronic disease management involves treating the complications e.g., heart failure
Clinical features of Chaga’s disease (Trypanosoma Cruzi)
mainly affects the heart and gastrointestinal tract
- myocarditis may lead to dilated cardiomyopathy (with apical atophy) and arrhythmias
- gastrointestinal features includes megaoesophagus and megacolon causing dysphagia and constipation
Most common cause of immune reconstitution syndrome (IRIS) in HIV
tuberculosis
How can IRIS can be distinguished from ARV failure
by monitoring response to treatment- typically patients with IRIS will have low viral loads and higher CD4 counts whereas in treatment failure high viral load and low CD4 count would be typical.
Syphillis Incubation Period?
How long to second phase?
How long to third phase?
1) Incubation period: 9-90 days
2) 6-10 weeks after primary infection
3) Years
Features of Primary Syphillis
chancre - painless ulcer at the site of sexual contact
local non-tender lymphadenopathy
often not seen in women (the lesion may be on the cervix)
Features of secondary Syphillis
Secondary features - occurs 6-10 weeks after primary infection
systemic symptoms: fevers, lymphadenopathy
rash on trunk, palms and soles
buccal ‘snail track’ ulcers (30%)
condylomata lata (painless, warty lesions on the genitalia )
Features of tertiary Syphillis
Tertiary features
gummas (granulomatous lesions of the skin and bones)
ascending aortic aneurysms
general paralysis of the insane
tabes dorsalis
Argyll-Robertson pupil
How to test for syphillis?
Cardiolipin tests
Syphilitic infection leads to the production of non-specific antibodies that react to cardiolipin. This reaction is the basis of traditional nontreponemal tests such as the VDRL test and rapid plasma reagin test.
examples include VDRL (Venereal Disease Research Laboratory) & RPR (rapid plasma reagin)
insensitive in late syphilis
becomes negative after treatment
Treponemal specific antibody tests
example: TPHA (Treponema pallidum HaemAgglutination test)
remains positive after treatment
Causes of 6 false positive cardiolipin (VRDL & RPR) tests
pregnancy
SLE, anti-phospholipid syndrome
TB
leprosy
malaria
HIV
Features of congenital syphilis
blunted upper incisor teeth (Hutchinson’s teeth), ‘mulberry’ molars
rhagades (linear scars at the angle of the mouth)
keratitis
saber shins
saddle nose
deafness
Treatment of syphillis
intramuscular benzathine penicillin is the first-line management
alternatives: doxycycline
the Jarisch-Herxheimer reaction is sometimes seen following treatment
fever, rash, tachycardia after the first dose of antibiotic
in contrast to anaphylaxis, there is no wheeze or hypotension
it is thought to be due to the release of endotoxins following bacterial death and typically occurs within a few hours of treatment
No treatment is needed other than antipyretics if required
What is Jarisch-Herxheimer reaction?
Within 24 hours after antibiotic treatment of the spirochetal infections syphilis, Lyme disease, leptospirosis, and relapsing fever (RF), patients experience shaking chills, a rise in temperature, and intensification of skin rashes known as the Jarisch–Herxheimer reaction (JHR) with symptoms resolving a few hours later.
Symptoms
fever, rash, tachycardia after the first dose of antibiotic
in contrast to anaphylaxis, there is no wheeze or hypotension
it is thought to be due to the release of endotoxins following bacterial death and typically occurs within a few hours of treatment
No treatment is needed other than antipyretics if required
