UTI and vector borne infections

• effects females more

• acute and short lived but can cause morbidity

• community or hospital acquired - less common than community

• many caused by E.coli

UTI settings of epidemology

• disrupts normal urine flow and complete bladder emptying

• allows microrganisms to access the bladder

• short female urethra - more prone to infection and harm

• caused by pregnancy, catheter, neurological bladder control symptoms

pathogenesis of UTI

• urethers

• urinary bladder and urethra

• dysuria, more urgency and frequency or urination

• those with cathethers and elderly can be asymptomatic

• cloudy urine due to bacteria and immune cells

acute UTI

• most urethers and kidney

• kidney infection - pyelonephritis

• fever

• more recurrent

• damage to renal tissue leading to hypertension, more kidney damage

• renal stones cause obstruction

• possible septicemia

upper UTI

• bacteurina - testing bacteria in the urine - mid-stream urine test

• most UTI resolve 2-4 weeks, antibiotics reduce symptoms

Lab diagnosis and treatment for UTI

• sexual behaviour – having more opportunities to control 

• asymptomatic

• those who have a high amount of sexual partners are prone

• different sexual practises can affect the throat and prostate

STI

• Syphilis

• thin, Gram-negative spirochete

• world wide risk

• rise over last 5 years

• enters the body through minute abrasions on the skin/mucous membranes

• transmit via sexual contact or vertical transmission - mother to fetus

• doesnt survive well outside body

• has a lipid coating which cant be detected by immune cells - antigentic unreactive

Treponema pallidum

• primary - slow proliferation of treponemas at site of infection; forms chancre: a firm, painless, non-itchy skin ulceration and proliferate in the regional lymph nodes for 1-3 months

• secondary stage - further multiplication and lesions in lymph node, liver, joint, muscle, skin and mucous membranes. Diffuse rash, frequently involving palms of the hands, soles of the feet, vagina and mouth sores - headache, myalgia and fever, can remain dormant in liver and spleen for up to 3-30 years

• tertiary - progressive destructive disease, soft tumour like and effect skin, bones and liver

Syphilis stages

• fetus wont contract it if mother is treated early

• spontaneous abortion, still birth, premature

• congenital abnormalities at birth or silent and develop after 2 - tooth or facial deformities

Congenital syphilis

• serologic tests are needed to confirm diagnosis

• can differentiate between other STIs

• Confirmation with dark-field microscopy or immuno-fluorescent labelling

• congenital - prevented if treated early with pencillin before 3 months of pregnancy

syphilis detection

• Penicillin very effective

• early diagnosis need to prevent from becoming secondary or tertiary

syphilis treatment

• Gram-negative dipoccocci

• Only infects humans – usually close contact (sexual contact)

• does not survive well outside body

• vertical transmission - mother to baby

• asymptomatic

• common in women

Neisseria gonorrhoeae

• usually via the vagina/’urethral mucosa of the penis can also attach to throat or rectal mucosa

• adherance factors prevent the bacteria fromm being washed away by urine/vaginal discharges

• capsule to resistance phagocytosis

• pilli for attachment to the membrane

• Por proteins which are antigenic surface protein for different serotypes

• rapidly multiply and spread through the cervix or up the urethra in men

• IgA protease - to destroy IgA

Gonoccoci virulence factors

• Invade non-ciliated epithelial cells

• multiply inside tiny protective vacuoles intracellularly - protecting it from phagocytes and antibodies

• Vacuoles discharges bacterial into sub-epithelial connective tissues allowing it to travel to deeper epithelial layers

• Lipolysaccharide causes a massive inflammatory response

• usually localised by it can spread to the bloodstream

Pathogenesis of Gonoccocci

• 2-7 days

• urethral discharge and pain on passing urine (dysuria) in men

• vaginal discharge in women

• mild or asymptomatic

• if untreated can lead to pelvic inflammatory disease, chronic pelvic pain, infertility - fallopian tube damage

Gonorrhoea clincal features

• analysing the microscopy and culture of urethral/vaginal discharges, combine with symptoms

• treated with antibacterials - cephalosporins

• pencilin resistance forms - penicillinase-producing N. gonorrhoeae

• resistance to fluoroquinolones

Gonnorrhea diagnosis and treatment

• Gram-negative

• ovoid in shape

• very small

• obligate intracellular parasite

• non-motile

• different serotypes by different infections

• transmitted via sexual intercourse

• asymptomatic in women

• vertical transmission - risk of pneumonia and ocular infection

Chlamydia trachomatis

• enters through minute abrasions in mucosa

• 1. Elementary body - extracellular survival and infection - enters target cell by triggering endocytosis, and prevents fusion of endosome with lysosome, preventing it from being degraded, once in the endosome it produced glycogen to germinate and form reticular body

• 2. Reticular body - vegetative form, proliferates rapidly after it proliferates it is converted back into the elementary body which is exocytosis and allows it to infect other cells, inflammation and damage

Chyamadia life cycle

• Clinical features are not distinctive

• PCR testing

• Microscopy with specific fluorescent antibodies

• Isolation and culturing in tissue culture to detect the inclusion bodies

• Microscopy with specific fluorescent antibodies

Detection of chlamydia

• Doxycycline or azithromycin

• Erythromycin should be used for babies of infected mother

• Early detection and treatment to reduce and avoid complications

Chlamydia treatment

• lentivirus - meaning slow

• Enveloped, ssRNA

• Retrovirus

• non-oncogenic but can kill cells

• genetically variable

• able to converts it RNA genome into DNA copy which can be integrated into the host cell to become a provirus

• variety of genomes can be found in the same person - people can respond differently to treatment and makes it hard to treat

Human immunodeficiency virus features

• gag - capsid matrix protein

• pol - reverse transcriptase

• env - envelope proteins - gp120 (binding to host cell) and 41

• env gene is highly variable - hampers vaccine development

• HIV 1 - worldwide, HIV 2 - africa and less pathogenic

• cross species infection

HIV viral features

• gp120 protein binds to CD4 molecules and a chemokine receptor

• g41 protein enable fusion with cell membrane or endocytosis

• integration - viral reverse transcriptase copies viral RNA genome into DNA

• cell machinery produces RNA transcripts of viral genome and necessary proteins

• Virions exit through exocytosis

HIV replication cycle

• the virus (either as free floating virus particles or carried inside an already infected cell) breaches the body's mucosal barrier lining.

• Dendritic Cells (DCs) and macrophages identify the virus in the underlying tissue

• and present it to CD4 + T cells

• the virus infects the active CD4+ T cells allowing it to produce mutiple copies of the virus and dormant CD4+ T cells allowing to be undetected by the immune system

• immune system activates Cytotoxic T Lymphocytes work to kill the infected cells

• however they only kill the CD4+ T cells which are active leaving the dormant ones, allowing it to remain in the body like in the lymphoid tissue and regulatory T cells supress the immune response

HIV pathogenesis

• Primary - 2-4 weeks, fatigue rash, headache, nausea, night sweats

• asymptomatic but still infectious - 10 years

• Untreated can lead to AIDS (Acquired immunodefiency syndrome) - destruction of many helper t cells - allowing them to develop opportunistic infections such as candida, hepatitis b

• also prone to cancerous viral infections - Burkitts lymphoma, Epstein Barr Virus

Clinical feature of HIV

• sexual or oral sex contact

• contaminated parenteral exposure

• transmitted via breastfeeding or birth

• not transmitted via casual contact

• inactivated in 10mins in room temp and disinfected by bleach

HIV transmission

• Highly active anti-retroviral therapy (HAART) - mixture of anti-viral reagents - prolongs a person’s survival, no HIV eradication

• Nucleoside analogues and non-nucleoside inhibitors for reverse transcriptase

• Viral protease inhibitors, integrase inhibitors, fusion inhibitors

• reduces transmission from mother to infant

• no vaccine

• expensive - not for developing countries

HIV treatment

• number of infectious diseases are transmitted to humans by blood-feeding

  arthropods

• viruses and parasites, mosquitoes

Vector borne infections

• transmission in areas of a small population

• parasite to vector to humans

• need to be able to have the opportunity to transmit, evading immune response of the host, survival within the host and vector must be alive to transmit to the host

Transmission of disease by vectors

• The parasite needs to be able to transmit into the host at the right place and the right time

• The parasite must be able to evade the immune responses of the host

• The parasite must be able to survive in the host and the vector without death and especially be able to pass the parasite before it dies.

challenges of vector borne

• transmitted by ticks, mosquitoes and sandflies

• can cause mild, haemorrhagic, prolonged fever or encephalitis

• e.g. Hameorrhagic fever, Dengue, Japanese encephalitis

Arboviruses

• human, vector, human - reservoir host from human and vector - dengue

• animal, vector, human - animal to vector, reservoir host is in animal, human become infected - japanese encephalitis

Arbovirus transmission cycle

• mild or subclinical - result in haemorrhagic disease or encephalitis

• No antiviral treatment is available

• Diagnosis is by virus isolation or measurement of antibodies

• Dengue and ross river - most common

• some vaccines avaliable

Arboviruses causing fever and haemorrhage

• mostly rapid and emerging

• Southeast Asia, Pacific Region, India, South and Central America

• Aedes aegypti mosquito - vector

• 4-8 incubation days

• malaise, fever, headache, erythematous rash

• no antiviral, NSAID cant be used

Dengue fever

• Infected person has acute symptoms when there is a high level of the virus in

  the bloodstream.

• immune response fights the infection, the person’s B cells begin producing

  IgM and IgG antibodies that are released in the blood and lymph fluid,

• Dengue virus and viral molecules are recognised and neutralised

• Virus is eliminated leading to recovery

Immune response to dengue

• severe

• caused by 4 different serotypes

• re-infection with a different serotype will result in enhanced iinfection capacity and increased infection efficiency

• high density of infected monocytes results in increased release of cytokines which leads to vascular damage, shock and haemorrhage in gastrointestinal tract and skin

• vomiting of blood, weak and rapid pulse

Dengue haemorrhagic fever

• topical infectious disease

• transmission of Plasmodium protozoa

• mainly P. falciparum

• children under 10, immuncompromised and pregancy are at risk

• high in african region

Malaria

• infects the infective form - sporozite into the blood and infects and matures in the hepatocyte

• Inside the liver cells, they multiply massively until the cells burst open, releasing thousands of new parasite forms (merozoites) into the bloodstream

• parasites invade red blood cells, transforming into a distinctive shape

• multiply inside the red blood cells until the cells burst

• bursting releases more parasites to infect new red blood cells, triggering the classic malaria symptoms like severe chills and fevers.

• some parasites in the blood stop dividing asexually and develop into male and female sexual forms - gametocytes

• when a new mosquito arrives it sucks up these gametocytes, reproduction occurs in the gut and then goes to infect another host

Malaria life cycle

• uncomplicated - High fever, chills, profuse sweating,

• severe - altered consciousness, lethargy or coma, breathing difficulties, severe anaemia

• P. falciparum - can be fatal 2 weeks after symptoms develop if untreated - leading to cerebral malaria

  severe anaemia and acute renal failure

• others a benign and self-limiting

clinical features of malaria

• highly complex and multifactorial immune response

• complex, multi-stage life cycle and expresses a large variety of proteins at different stages, and these proteins often change

immune response to malaria

• rapid detection tests

• PCR

• clinical examination

• rapid diagnostic

• combines a fast and slow acting drug for uncomplicated malaria

• intravenous or intramuscular artesunate  for 24hr until oral therapy can be tolerated

treatment and diagnosis for malaria

malaria treatment

• microscopic, one-celled organisms

• live in blood or tissue t

• transmitted by an arthropod vector

• sub-african

Protoza infections

• multicellular eukaryotic invertebrates with tube- like or flattened bodies exhibiting bilateral symmetry

• unlike other pathogens, helminths do not proliferate within the host develop slowly (compared to other infectious agents)

• slow onset and chronic in nature

Helminth infections

• Parasitic disease

• endemic to Africa, South America, China and Southeast Asia

• infection with blood flukes of the genus Schistosoma

• second largest socioeconomic impact, after malaria

• changing patterns of travel and migration

Schistosomiasis

• contamination of the water

• enters the vector of a fresh water snail

• inside the snail, the parasite multiplies and releases free-swimming

• human swims or wades in the contaminated water, these cercariae burrow directly through the skin, shedding their tails as they enter

• they travel through the blood vessels, passing through the lungs and liver

• migrate to veins surrounding the bladder or intestines and mature into adult male and female worms, and begin laying thousands of eggs

• sharp eggs penetrate the walls of the bladder or bowel and leave the human body through urine or stool

Schistosomiasis life cycle

• invasion leads to dermatitis

• Fluke maturation leads to allergic response

• Egg laying leads to inflammation and haemorrhage

• eggs become trapped in organs (liver, lungs,severe inflammatory responses can occur

• treatment can cause more severe symptoms

• fever, non-productive cough, eosinophilia and gastrointestinal symptoms

Schistosomiasis clinical features

• low helper T cell 1 response initally

• then as eggs develop and adult worms form the helper T cell 1 response increases

• regulatory T cell response increases as eggs develop

immune response to schistosomiasis

• Microscopic examination of urine or faeces - samples collected between 10-2pm

• ova may not be detected until 6 weeks after exposure

• serology - antibody not detected until 4-12 weeks after infection

• treatment - 2 doses of praziquantal given 4 hours apart

schistosomiasis diagnosis and treatment