Arthropods can transmit viruses, bacteria and parasites. To date, there is no known arthropod-borne fungal infection.

Mosquitoes transmit more disease, and a greater variety of disease, than any other arthropod. However, other biting flies, fleas, ticks, lice and mites are also responsible for transmission of some infections. Most of these infections are zoonotic; animal and human hosts may exhibit disparate behaviour and inhabit differing environments, thus the arthropod vector is essential at bridging the ecological gap between the two. Arthropod-borne animal infections may adapt to transmit to humans and directly from human to human, making arthropods important contributors to the emergence of some infectious diseases.

Some mosquito species, such as Aedes (Stegomyia) aegypti , are increasingly cosmopolitan and are found throughout the tropical world. The ability of Ae. (Stg.) aegypti to breed in dirty urban water containers has resulted in large outbreaks of dengue in tropical metropolises. Rapid airline transport of mosquitoes or infective human hosts may result in large outbreaks of disease in areas previously free of infection but with competent arthropod vectors. South America has been afflicted by this twice in the last 5 years; chikungunya arrived in 2013 and Zika virus in 2015.

Some pathogens, particularly parasites, are dependent upon arthropod host physiology to complete their life cycle. Most pathogens can multiply within the arthropod vector and some, particularly viruses, may mutate to more virulent or transmissible forms of disease. A single nucleotide polymorphism in Venezuelan equine encephalitis virus increased its infectivity to Culex , resulting in an outbreak of disease in Mexico in 1996.

With the exception of Japanese encephalitis and yellow fever, there are few effective vaccines for arthropod-borne diseases. At the community level, prevention relies upon vector control through environmental management and chemical agents. In recent years, there has been increasing insecticide resistance worldwide, threatening control programmes. There is also increasing resistance to essential drugs used to treat these diseases, such as artemisinin which is used to treat malaria.

This chapter is divided into four sections. The first describes the main mosquito vectors of infection and the following three sections describe arthropod-borne viral, bacterial and parasitic infections.

Mosquito Vectors

The main characteristics of the principal mosquito vectors of infection are presented in the following figures.

Fig. 1.01, Mosquito life cycle.

Fig. 1.02, Female Anopheles gambiae probing.

Fig. 1.03, Aedes (Stegomyia) aegypti taking a blood meal.

Fig. 1.04, Aedes (Stegomyia) albopictus taking a blood meal.

Fig. 1.05, The expanding geographical range of Aedes (Stegomyia) albopictus .

Fig. 1.06, Feeding Culex pipiens.

Fig. 1.07, Anopheles eggs.

Fig. 1.08, Aedes (Stegomyia) eggs.

Fig. 1.09, Culex eggs.

Fig. 1.10, Third-stage larva of Anopheles spp.

Fig. 1.11, Third-stage larvae of Culex quinquefasciatus and Aedes (Stegomyia) aegypti .

Fig. 1.12, Pupae of Anopheles spp.

Fig. 1.13, Heads of adult culicine mosquitoes.

Fig. 1.14, Heads of adult Anopheles mosquitoes.

The Arboviruses: Arthropod-Borne Viral Infections

The arboviruses are a diverse group of viral infections spread by arthropods. Following a blood meal from an infected vertebrate host, the virus multiplies within the arthropod, before being transmitted to a vertebrate host.

Most arboviruses are zoonotic; the exceptions are dengue and o’nyong’nyong where humans are the primary vertebrate host. Mosquitoes are the most common vectors, but ticks and sandflies are also implicated in the transmission of some viruses. The global distribution of some mosquito vectors and the rapidity of international travel has allowed certain viruses to become endemic in areas previously free of disease following movement of viraemic hosts or mosquitoes. Gene mutation may also have an effect on transmission; chikungunya moved rapidly through Asia following a single amino acid change in its envelope protein, which greatly increased transmissibility by a secondary mosquito vector, Aedes (Stegomyia) albopictus .

Although arboviruses cause a wide range of clinical symptoms, it is conceptually simpler to consider them in syndromic groups. Some, such as dengue and chikungunya virus, cause a fever, arthralgia and rash syndrome. Others, such as West Nile virus and St Louis encephalitis virus, cause an encephalitic syndrome. Viruses such as Crimean-Congo haemorrhagic fever and yellow fever may cause a haemorrhagic syndrome. There is some overlap between these syndromic groups; West Nile virus causes fever, arthralgia and rash in mild infection and encephalitis in severe infection. Table 1.1 summarises current arboviruses of clinical significance, updated to December 2016.

Table 1.1
Arboviruses of clinical significance, updated to December 2016
Virus or disease Main vector(s) Main reservoirs/amplifying hosts Geographical distribution Clinical syndrome
Family: Togaviridae
Genus: Alphavirus
Chikungunya Aedes Monkeys, ? rodents Africa, Asia, South America FAR
Mayaro Aedes, Anopheles Wild vertebrates South America FAR
O'nyong'nyong Anopheles Humans Africa FAR
Ross River Aedes ? Wallabies Australia FAR
Sindbis Culex Birds Africa, Asia, Australia, Europe FAR
Venezuelan equine encephalitis Aedes, Culex Rodents/horses North/South America Encephalitis
Western equine encephalitis Culex Birds/horses North/South America Encephalitis
Eastern equine encephalitis Culiseta Birds/horses North/South America Encephalitis

Family: Flaviviridae
Genus: Flavivirus
Dengue 1, 2, 3, 4 Aedes Aedes/humans Worldwide tropics FAR
Zika Aedes Humans/non human primates Africa, South America, Asia, Pacific FAR, congenital syndrome
Kunjin Culex Birds Australia, Indonesia FAR/encephalitis
Japanese encephalitis Culex Birds/pigs East Asia/Australasia Encephalitis
Murray Valley encephalitis Culex Birds Australia Encephalitis
Rocio Culex Birds Brazil Encephalitis
St Louis encephalitis Culex Mosquitoes, birds North/South America Encephalitis
West Nile Culex Birds, bats, horses, Africa, Europe, North America, Middle East Encephalitis
Louping ill Ixodidae Rodents, birds UK Encephalitis
Powassan Ixodidae Rodents North America Encephalitis
Tick-borne encephalitis Ixodidae Small mammals/ruminants Europe Encephalitis
Russian spring-summer encephalitis Ixodidae Rodents, birds Russia Encephalitis
Kyasanur forest disease Ixodidae Forest rodents/monkeys India Haemorrhagic
Omsk haemorrhagic fever Ixodidae Ticks, rodents Russia Haemorrhagic
Yellow fever Aedes
Haemagogus
Mosquitoes/monkeys South America, Africa Haemorrhagic

Family: Reoviridae
Genus: Coltiviridae
Colorado tick fever Ixodidae Rodents North America FAR/encephalitis/haemorrhagic

Family: Bunyaviridae
Genus: Nairovirus
Crimean-Congo haemorrhagic fever Ixodidae Ticks, sheep, goats, cattle, rodents, birds Parts of Africa, Asia, Europe, Middle East, Haemorrhagic
Genus: Bunyavirus
California encephalitis group Aedes Rabbits, rodents North America Encephalitis
La Crosse Aedes Chipmunks, squirrels North America Encephalitis
Oropouche Culicoides Monkeys, sloths South America FAR, encephalitis
Genus: Phlebovirus
Rift Valley fever Anopheles, Aedes, Culex Cattle, sheep, goats Africa, Middle East Fever, encephalitis, haemorrhagic
Sandfly fever (Naples, Sicily) Phlebotomus Unknown Africa, Asia, Europe FAR
Sandfly fever (Toscana) Phlebotomus Unknown Countries bordering Mediterranean Sea FAR, encephalitis

FAR: fever, arthralgia, rash syndrome

Dengue

Fig. 1.15, Worldwide distribution of dengue.

Fig. 1.16, Breeding site of Aedes (Stegomyia) aegypti in a Thai cemetery.

Fig. 1.17, Clinical course of dengue infection.

Fig. 1.18, Typical dengue rash.

Fig. 1.19, Confluent rash with islands of sparing.

Fig. 1.20, Linear petechiae in a patient with dengue.

Fig. 1.21, Subcutaneous haemorrhage in dengue haemorrhagic fever.

Fig. 1.22, Intracranial haemorrhage in severe dengue.

Fig. 1.23, Dengue point-of-care test.

Fig. 1.24, Guppy fish used for vector control in South East Asia.

Yellow Fever

Fig. 1.25, The distribution of yellow fever.

Fig. 1.26, Transmission cycles of yellow fever.

Fig. 1.27, Temperature chart of a patient with yellow fever.

Fig. 1.28, Upper gastrointestinal bleeding in the terminal phase of yellow fever.

Fig. 1.29, Section of liver from a fatal case of yellow fever.

Fig. 1.30, Angolan child vaccinated during the 2016 yellow fever outbreak.

Chikungunya and Other Alphaviruses

Fig. 1.31, Acute arthritis of the interphalangeal joints in a patient with chikungunya.

Fig. 1.32, Eastern grey kangaroos, vertebrate host of Ross River virus.

Fig. 1.33, MRI changes in a fatal case of eastern equine encephalitis.

Zika

Fig. 1.34, Rash of Zika virus.

Fig. 1.35, Brazilian infant with microcephaly.

Fig. 1.36, CT scan abnormalities in congenital Zika virus syndrome.

Fig. 1.37, Urine and semen; diagnostic specimens for Zika virus polymerase chain reaction.

Japanese Encephalitis and West Nile

Fig. 1.38, Geographical distribution of the West Nile and Japanese encephalitis viruses.

Fig. 1.39, Grey heron, a potential carrier of West Nile virus (WNV).

Fig. 1.40, Maculopapular rash in West Nile virus (WNV).

Fig. 1.41, A section of human brain from a fatal case of encephalitis caused by West Nile virus (WNV).

Fig. 1.42, MRI of an immunocompromised patient with West Nile virus (WNV).

Fig. 1.43, Control of culicine vectors of West Nile virus (WNV).

Fig. 1.44, Blood transfusion.

Fig. 1.45, Cycle of transmission of Japanese encephalitis virus (JEV).

Fig. 1.46, Culex tritaeniorhynchus .

Fig. 1.47, Rice paddy fields in South India.

Fig. 1.48, Acute Japanese encephalitis.

Fig. 1.49, Wasting following acute flaccid paralysis secondary to Japanese encephalitis virus (JEV).

Fig. 1.50, MRI changes in acute Japanese encephalitis virus (JEV).

Rift Valley Fever and Crimean-Congo Haemorrhagic Fever

Fig. 1.51, Distribution of Rift Valley fever virus (RVFV) and Crimean-Congo haemorrhagic fever (CCHF).

Fig. 1.52, Farmer with cattle in East Africa.

Fig. 1.53, Retinitis in a patient with Rift Valley fever virus (RFVF).

Fig. 1.54, Hyalomma marginatum .

Fig. 1.55, Immature Hyalomma marginatum rufipes feeding on an African dove, Streptopelia senegalensis .

Fig. 1.56, Ecchymoses in a patient with Crimean-Congo haemorrhagic fever.

Fig. 1.57, Bilateral subconjunctival haemorrhage.

Fig. 1.58, Subarachnoid haemorrhage in a patient who died of Crimean-Congo haemorrhagic fever.

Arthropod-Borne Bacterial Infections

Arthropod-borne bacterial infections are predominantly transmitted by ticks, lice, mites and fleas. The exception to this is Francisella tularensis, which can be transmitted by mosquitoes, and Bartonella bacilliformis, which is believed to be transmitted by sandflies.

Rickettsiae multiply within vascular endothelial cells resulting in a vasculitis-like systemic disease of varying severity. These infections are summarized in Table 1.2 . Borrelia species are expert at evading the immune system; B. burgdorferi is one of medicine’s great imitators whilst episodic antigen variation in other Borrelia species gives rise to periodic fever relapses. Yersinia pestis has caused some of the greatest plagues in history, including the Black Death, which killed up to 200 million people between 1346 and 1353.

Table 1.2
Clinically relevant rickettsial diseases, updated to 2016
Disease Causative agent Vector Animal reservoir Geographical distribution
Typhus
Epidemic typhus Rickettsia prowazekii Pediculus humanus corporis Humans
Flying squirrels– New World
Unclear elsewhere
Ethiopia/Rwanda/Burundi
Rural South/Central America
Endemic (murine) typhus Rickettsia typhi Xenopsylla cheopis
Ctenocephalides felis
Rat
(cat, opossum-USA)
Worldwide
Spotted fevers
Rocky Mountain spotted fever Rickettsia rickettsii Various tick spp. Many small mammals North America, patchy distribution in Central and South America
Mediterranean spotted fever/Fièvre boutonneuse Rickettsia conorii Rhipicephalus sanguineus Dogs, small mammals Mediterranean, sub-Saharan Africa
African tick typhus Rickettsia africae Amblyomma spp. ? Rodents Sub-Saharan Africa, Eastern Caribbean
Lymphangitis associated rickettsiosis Rickettsia sibirica subsp mongolotimonae Dermacentor spp. Farm and wild animals France, Portugal, South Africa
Transitional group rickettsiae
Queensland tick typhus Rickettsia australis Ixodes holocyclus Rodents Australia
Rickettsial pox Rickettsia akari Mites
Liponyssoides sanguineus
Mice Korea, central and southern Africa, Ukraine, eastern USA
Scrub typhus
Scrub typhus Orientia tsutsugamushi Trombiculid mites Small mammals, rodents, birds South and South East Asia, Australia, Pacific
Anaplasmosis
Human monocytic ehrlichiosis Ehrlichia chaffeensis Amblyomma americana White tailed deer, raccoon, opossum Unclear – cases reported from North America, Europe, Asia, Africa
Human granulocytic anaplasmosis Anaplasma phagocytophila Ixodes scapularis White-footed mouse, other rodents, cattle, sheep, horses North America, North and Central Europe, China, Russia

Vertical transmission can occur in vectors.

Table 1.3
The filarial diseases
Species Clinical disease Location of MF (periodicity) Sheath Main characteristcs Distribution
Wuchereria bancrofti LF Blood
(nocturnal )
+ Tail - pointed tail, nuclei not to tip. Body - 275-300 x 9μm, smooth curves. Sheath - stains pale mauve with Giemsa.

All tropics
Brugia malayi LF Blood
(nocturnal ∗∗ )
+ Tail - tapers irregularly, 2 nuclei at tip.  Body - 200-275 x 6μm, kinked.  Sheath - stains bright pink with Giemsa.

Southeast Asia
Brugia timori LF Blood
(nocturnal)
+ Tail - tapers irregularly, 2 nuclei at tip. Body - 290-325 x 6μm, kinked. Sheath - stains poorly with Giemsa.

Timor-Leste
Loa loa Eye worm Blood
(diurnal)
+ Tail - rounded tip, nuclei to tip. Body - 250-300 x 9μm, kinked. Sheath - does not stain with Giemsa.

West Africa, forested areas
Onchocerca volvulus River blindness Skin
(no periodicity)
Tail - long and pointed, nuclei not to tip, crooked.  Body - 240-360 x 8μm.  Head - spatulate. No sheath.

Africa, Central and South America, Yemen
Mansonella perstans Most asymptomatic Blood
(no periodicity)
Tail - nuclei extend to tip of rounded tail, large nucleus at tip.  Body - 190-240 x 5μm. No sheath. Sub-Saharan Africa, Central and South America
Mansonella ozzardi Most asymptomatic Blood/Skin
(no periodicity)
Tail - long pointed tail with no nuclei. Body - 150-200 x 5 μm, anterior nuclei positioned side by side. No sheath. Central and South America, Caribbean
Mansonella streptocerca Asymptomatic
Dermatitis
Skin
(no periodicity)
Tail - nuclei extend to tip of rounded, hooked tail. Body - 180-240 x 5μm. Single file anterior nuclei. No sheath.

Central and West Africa
LF , lymphatic filariasis.

In the South Pacific, microfilariae may be diurnally sub-periodic.

∗∗ In the Philippines, microfilariae may be nocturnally sub-periodic.

All of these bacteria are capable of causing severe disease, requiring antibiotics for resolution. Most respond to doxycycline, although the addition of further agents including aminoglycosides or chloramphenicol is often beneficial.

Typhus

Fig. 1.59, Refugees in the Ethiopian Highlands.

Fig. 1.60, Feeding body lice ( Pediculus humanus corporis ).

Fig. 1.61, Rash of epidemic, louse-borne typhus (R. prowazekii) .

Fig. 1.62, Peripheral gangrene in severe epidemic typhus.

Fig. 1.63, Rattus norvegicus, a host of Rickettsia typhi (murine typhus).

Spotted Fevers

Fig. 1.64, Male and female Amblyomma variegatum , a vector of Rickettsia africae in sub-Saharan Africa (M - left, F - right).

Fig. 1.65, Eschar of African tick typhus.

Fig. 1.66, Petechial rash of Rocky Mountain spotted fever (RMSF).

Fig. 1.67, Rickettsia sibirica .

Fig. 1.68, Scalp eschar in a patient with Rickettsia slovaca infection.

Fig. 1.69, Eschar and vesicular rash of Rickettsia akari .

Fig. 1.70, Liponyssoides sanguineus .

Scrub Typhus

Fig. 1.71, Distribution of scrub typhus.

Fig. 1.72, Larva of Leptotrombidium .

Fig. 1.73, Longitudinal section through a feeding trombiculid larva to show the stylostome.

Fig. 1.74, Eschar at site of mite bite.

Fig. 1.75, Acute respiratory distress syndrome (ARDS) in a patient with severe scrub typhus.

Fig. 1.76, Intraleukocytic inclusion body (morula) of Anaplasma phagocytophilum causing human granulocytic anaplasmosis.

Bartonella

Fig. 1.77, Blood film showing Bartonella bacilliformis in Carrión’s disease.

Fig. 1.78, Lesions of ‘verruga peruana’.

Fig. 1.79, Bacillary angiomatosis.

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