Apiculture and Wildlife: T3: Diseases of Bees

Healthy Brood

Healthy Brood

Larvae are pearly white and glistening

Brood pattern is solid & sweetish color of honey

Cappings ar dry, slight convex and no perforation

Infected Brood

Infected/dead larvae - dirthy white to brownish color

Brood pattrn is scattered or spotty

Cappings are moist, sunken & perforated

Healthy Adult Bees

Active and busy at work

intack wings

strong population

complete age from newlyemerged to forager bees

Infected Aadult Bees

Slow movers

weak population

body and wings are deformed

Varroa Maites

Greatest health threats faced by bees

Varroa Mites

Name after ancient roman scholar and bee keeper Marcus Terentius Varro

Varroa Jacobsoni

first mite species in Apis cerana colonies

Varroa destructor

in 1950 to 1960 bee keepers in the USSR and Philippines detected red mites infesting Apis mellifera

White remnants of feca pile on one of the cell walls

clearest indication that a cell has been used for mite reproducion

Inbreedig

mite reproduction

Female Varroa mites

all mites to be encoutered by a bee keeper will likelly be

Varroa Mites

Cs (colony)

High mortality at the hives entrance

rapid loss of adult bee popo=ulation, malnuorished, crawling and crippled bees (w/ deformed wings)

dead uncapped larvae, scattered brood

brood cells with wax capping fissured, sunken o partially removed or with white patched on the cell wall

supersedure of queen

Adult Varroa Mites appear

red to reddish brown ovals

Overlapping exoskeletal plates/ sclerites

where the varroa mites insert themselves

Varoosis

diseased state of heavily mite infested colonies

Varoosis

commonly known as “collapsing due to mites”

Varroa Mites

Cx (individual)

injuries in the cuticle

depletion of haemolymph and fat body tissue

impairment of the immune system

reuction of size and weight of hatching honey bees

Parasitized Worker bees by Varroa Mites

have shorter lifespan, forages earlier and have reduced capacity for no-associative learnig, orientation and homing ability

Parasitised Drone bees by Varroa Mites

decreased flight performance ans shorter lifespan, sperm production is reduced

Varroa Mites Treatment

Chemical: miticides (formic acid, oxalic acid, amitraz, coumaphos)

Nonchemical: brood interuption, drome comb removal. screem bottom boards

Iflavirius aladeformis

Deformed wing virus

deformed wing virus

first found in adult honey bees in egypt

named egypt bee virus (EBV)

Deformed wing virus

causes overt sysptom of misshapen and crippled wings of heavily infected worker bees

deformed wing virus / iflavirius aladdeformis

ubiquitous, one of the most prevalent viral pathogens of honey bees

affects all honey bee parts, case and developmental stage

deformed wing virus

transmission: vertically and horizontal

Deformed wing virus

cx:

pupal dealth

shrunken, crumpled wings

bloated abdomen

decreased body size

discoloration in newly emerged bees

infected bees are slower to emerge

hypoplasia of the hypopharyngel and mandibular glands

ovarian degredation

sacbrood virus

Morator aetatulas

sacbrood virus

first virus to be describes in A. mellifera

sacbood virus

first honey bee virus to have its complete genome sequenced and assemled, nearly unbiquitous

sacbrood disease

frequently detected from seemingly healthy adult quees, drones, and worker bees as latent infection

sacbrood virus

accumulates in the hypopharyngea glands (nurse bees)

sacbrood virus

varroa mites serves as mechanical vectors

sacbrood virus

transmission: horizontally thru nurse bees feeding larvae or exchanging food with other adult bees

sacbrood virus

cx:

diseased larvae and its ushed cuticle for a sac-like appearance

infected brood failsto populate , are stretched on their backs with heads lifted up toward the cell openinf

sacbrood on A. mellifera

mild, larval death and colony depopulation

sacbrood on A. cerana

serious colony collapse

slow bee paralysis virus

first discovered in 1974 in the united kingdom

slow bee paralysis

transmission: orally by varroa mites directly to adults bees and pupae during parasitic feeding

slow bee paralysis

paralysis of the anterir two pair of the legs about 10-12 days after injection into the abdomen by adult bees

slow bee paralysis

High virus accumulation in the head (specifically the hypopharyngeal,
mandibular, and salivary glands), the fat body, the crop, and forelegs but less in the hindlegs, midgut, rectum, and thorax

black queen cell virus

family dicistroviridae, genus cripavirus

black queen cell virus

one of the most prevalent, yet least understood honey bee virus

black queen cell virus

detected from both european and asian honey bees

black queen cell virus

darkened areas of the wall of the queen cells containing infected pupae

black queen cell virus

most common cause of death of queen larvae

black queen cell virus

largely a gut pathogen that is often associated with N. apis

black queen cell virus

social transmission amoung adults and from adults to larvae through glandualr secretion. potential vertical transmission

acute bee paralysis virus

first discovered in 1963 as an asymptomatic infection during laboratory experiment

acute bee paralysis virus

largely horizontal intra-colony transmission and low inter-colony spread

acute bee paralysis virus

particularly virulent

the injection of 100 virions can cause death of pupae or adlts within 2-6 days

acute bee paralysis virus

resemble the symptom of certain bacterial disease

acute bee paralysis virus

transmission: orally (thru hypopharyngeal glands and feces f worker bees) potentia vertical transmission

acute bee paralysis virus

cx:

paralysis

trembling

inability to fly

gradual darkening and loss of hair from the thorax and abdomen

chronic bee paralysis virus

discovered in 1960s by leslie bailey

chronic bee paralysis virus

hairless black syndrome

chronic bee paralysis virus

transmission: secrete virus from it epidermis and feces, turining it into a mobile virus factory

Chronic bee paralysis virus Type 1

Symptoms:

abnormal trembling motion with paralysis of the wings and bodies

inability to fly and crawling

bees are misplaced in the hive, appearing on top bars and lugs

bloated abdomens

chronic bee paralysis virus type 2

hairless bees, appearing almost black and shiny, greasy bees, suffering from nibbling attacks by healthy bees

european foulbrood (EFB)

caused by gram-positive, micriaerophiic, and lanceolate bacterium Melissococcus plutonius

all caste are affected

Melissococcus plutonius

previous name: Bacillus alvei, Bacillus pluton, Streptococcus pluton

M. plutonius

can be present inhives that are apparently healthy and show no sign of disease

occur in larval midgut

european foulbrood

transmission: infected adult beed carry the bacteria within the colony

robbing of honey

european foulbrood

cx:

imbalance between populations, spotty brood pattern

deficiency of pollen

sour, fish-like rotten odor

unever, spotty brood pattern or brood frams found n the outside frames in colony

grayish, withish-yellow to brown colored larvae

twisted and/or curled upward larvae with defined tracheal system that havewhite visible trachea

deflated larvae located at the bottom of the cell

may have roping, sticky larval remains at a maximu of 1.5 cm

brown to black hardened larvae “scales”, located at the bottom of the cells that are easy to move

american foulbrood

caused by gram positive, facultatuve anaerobic, endospore-forming bacterium Paenibacillus larvae

american foulbrood

young larvae ingest the spores of the bacterium which germinate in the honey bee’s gut

america foulbrood

majority of infected larvae die before capping and appear coiled in their cells

laboratory diagnosis

is the only accurate means to differentiate AFB and EFB

american foulbrood

transmission:

spores often occur during robbing

vertically through swarming

movement of equipment by beekeepers

american foulbrood

cx:

larvae are killed rapidly at early stages when they are curled aat the base of the uncapped brood cells

other larvae will die later on in theirdevelopment, when the are in a upright position, filling most of the brood cells

Spores of P. larvae

can survive in bee products and in the environmet for 3 to 10 years and for 35 years in dry larval scales. purified spores can survice even more than 70 years

3-4 years

brood combs should be replaced every ___ as old brood combs can act as reservoir of the bacterium of AFB

Chalkbrood disease

caused by fungus Ascosphaera apis

chalkbrood disease

kills the developing brood in the late stageproducing mummified and/or calcified larvae

Ingestion (chalkbrood disease)

spores of fungus enter the gut of a larva through

false skin (chalkbrood disease)

fungus hypahe extract nutrients from the larva and consume the rest of the host’s body, forming a

chalkbrood disease

cx:

young infected larvae usually dont show any signs

fungus-killed larvae shrink and dry to from a white or gray-black chalk-like mummy

brood pattern in the comb is scattered'

wax cell capping may also have small holes

chalkbrood disease

weakens a colony’s health, it rarely kills a colony